AiG - Genetics - DNA Similarities

Chapter 10
What About the Similarity Between Human and Chimp DNA?

by Dr. David A. DeWitt on January 14, 2014
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DNA similarity could easily be explained as a result of a common Creator.
The first thing I want to do is clear up a common misconception—especially among
many within the Church. Many falsely believe that in an evolutionary worldview
humans evolved from chimpanzees. And so they ask, “If humans came from chimps, then
why are there still chimps?” However, this is not a good question to ask because an
evolutionary worldview does not teach this. The evolutionists commonly teach that
humans and chimpanzees are both basically “cousins” and have a common ancestor in
our past. If you go back far enough, all life likely has a single common ancestor
in the evolutionary view. This, of course, does not mesh with Genesis 1–2.
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Evolutionists frequently assert that the similarity in DNA sequences provides
evidence that all organisms (especially humans and chimps) are descended from a
common ancestor. However, DNA similarity could just as easily be explained as the
result of a common Creator.
Human designers frequently reuse the same elements and features, albeit with
modifications. Since all living things share the same world, it should be expected
that there would be similarities in DNA as the organisms would have similar needs.
Indeed, it would be quite surprising if every living thing had completely different
sequences for each protein—especially ones that carried out the same function.
Organisms that have highly similar functionality and physiological needs would be
expected to have a degree of DNA similarity.
What Is DNA?
DNA
Figure 1. The double-stranded DNA molecule forms with an A opposite a T and a G

opposite a C. This sequence determines the structure of proteins.
Every living cell contains DNA (deoxyribonucleic acid), which provides the
hereditary instructions for living things to survive, grow, and reproduce. The DNA
is comprised of chemicals called bases, which are paired and put together in
double-stranded chains. There are four different bases, which are represented by
the letters A, T, C, and G. Because A is always paired with T and C is always
paired with G, one strand of DNA can serve as a template for producing the other
strand.
The DNA is transcribed into a single chain of nucleotides called RNA (ribonucleic
acid), which is then translated into the amino acid sequence of a protein. In this
way, the sequence of bases in DNA determines the sequence of amino acids in a
protein which in turn determines the protein structure and function.
In the human genome (total genetic information in the nucleus of the cell), there
are roughly three billion base pairs of DNA with about 20,000 genes (regions that
code for proteins). Surprisingly, only about 1 percent of the DNA actually codes
for proteins. The rest is non-coding DNA. Some of this DNA comprises control areas—
segments of DNA responsible for turning genes on and off, controlling the amount
and timing of protein production. There are also portions of DNA that play
structural roles. Still other regions of DNA have as yet unknown functions.
What Is the Real Percent Similarity between Humans and Chimpanzees?
Apes
Figures 2 and 3: Evolutionists believe that the similarity in the DNA sequence of
gorillas, chimpanzees, and humans is proof that they all share a common ancestor
(Photos: Shutterstock)
Ever since the time of Darwin, evolutionary scientists have noted the anatomical
(physical/visible) similarities between humans and the great apes, including
chimpanzees, gorillas, and orangutans. Over the last few decades, molecular
biologists have joined the fray, pointing out the similarities in DNA sequences.
Previous estimates of genetic similarity between humans and chimpanzees suggested
they were 98.5–99.4 percent identical.1
Because of this similarity, evolutionists have viewed the chimpanzee as “our
closest living relative.” Most early comparative studies were carried out only on
genes (such as the sequence of the cytochrome c protein), which constituted only a
very tiny fraction of the roughly three billion DNA base pairs that comprise our
genetic blueprint. Although the full human genome sequence has been available since
2001, the whole chimpanzee genome has not. Thus, much of the previous work was
based on only a fraction of the total DNA.
Nature magazine
Figure 4: The journal Nature often trumpets the common ancestry of humans and
chimps.
In the fall of 2005, in a special issue of Nature devoted to chimpanzees,
researchers reported the draft sequence of the chimpanzee genome.2 At the time,
some researchers called it “the most dramatic confirmation yet”3 of Darwin’s theory
that man shared a common ancestor with the apes. One headline read: “Charles Darwin
Was Right and Chimp Gene Map Proves It.”4
So what is this great and overwhelming “proof” of chimp-human common ancestry?
Researchers found 96 percent genetic similarity and a difference between us of 4
percent. This is a very strange kind of proof because it is actually double the
percent difference that evolutionists have claimed for years!5 Even so, no matter
what the actual percent difference turned out to be, whether 2, 4, or 10 percent,
they still would have claimed that Darwin was right to support their worldview.
Further, the use of percentages obscures the magnitude of the differences. For
example, 1.23 percent of the differences are single base pair substitutions (figure
5).6 This doesn’t sound like much until you realize that it represents about 35
million differences! But that is only the beginning. There are 40–45 million bases
present in humans that are missing from chimps and about the same number present in
chimps that are absent from man. These extra DNA nucleotides are called
“insertions” or “deletions” because they are thought to have been added to or lost
from the original sequence. (Substitutions and insertions are compared in figure
5.) This puts the total number of DNA differences at about 125 million. However,
since the insertions can be more than one nucleotide long, there are about 40
million total separate mutation events that would separate the two species in the
evolutionary view.
DNA Comparison
Figure 5: Comparison between a base substitution and an insertion/deletion. Two DNA

sequences can be compared. If there is a difference in the nucleotides (e.g., an A
instead of a G) at a given position, this is a substitution. In contrast, if there
is a nucleotide base that is missing it is considered an insertion/deletion. It is
assumed that a nucleotide has been inserted into one of the sequences or one has
been deleted from the other. It is often too difficult to determine whether the
difference is a result of an insertion or a deletion and thus it is called an
“indel.” Indels can be of virtually any length.
To put this number into perspective, a typical 8½ x 11-inch page of text might have
4,000 letters and spaces. It would take 10,000 such pages full of text to equal 40
million letters! So the difference between humans and chimpanzees includes about 35
million DNA bases that are different, about 45 million in the human that are absent
from the chimp, and about 45 million in the chimp that are absent from the human.
Creationists believe that God made Adam directly from the dust of the earth just as
the Bible says in Genesis 2. Therefore, man and the apes have never had an ancestor
in common. Assuming they did, for the sake of analyzing the argument, then 40
million separate mutation events would have had to take place and become fixed in
the population in only 300,000 generations. This is an average of 133 mutations
locked into the genome every generation. Locking in such a staggering number of
mutations in a relatively small number of generations is a problem referred to as
“Haldane’s dilemma.”7
The Differences Make the Difference
There are many other differences between chimpanzee and human genomes that are not
quantifiable as percentages.8 Specific examples of these differences include:
At the end of each chromosome is a string of repeating DNA sequences called
telomeres. Chimpanzees and other apes have about 23,000 base pairs of DNA at their
telomeres. Humans are unique among primates with much shorter telomeres only 10,000
long.9
While 18 pairs of chromosomes are virtually identical, chromosomes 4, 9, and 12
show evidence of being “remodeled.”10 In other words, the genes and markers on
these chromosomes are not in the same order in the human and chimpanzee. Instead of
being “remodeled,” as the evolutionists suggest, these could also be intrinsic
differences as each was a separate creation.
Even with genetic similarity, there can be differences in the amount of specific
proteins produced. Just because DNA sequences are similar does not mean that the
same amounts of the proteins are produced. Such differences in protein expression
can yield vastly different responses in cells. Roughly 10 percent of genes examined
showed significant differences in expression levels between chimpanzees and
humans.11
Gene families are groups of genes that have similar sequences and also similar
functions. Scientists comparing the number of genes in gene families have revealed
significant differences between humans and chimpanzees. Humans have 689 genes that
chimps lack and chimps have 86 genes that humans lack. Such differences mean that 6
percent of the gene complement is different between humans and chimpanzees,
irrespective of the individual DNA base pairs.12
Thus, the percentage of matching DNA is only one measure of how similar two
organisms are, and not really a good one at that. There are other factors besides
DNA sequence that determine an organism’s phenotype (how traits are physically
expressed). Indeed, even though identical twins have the same DNA sequence, as they
grow older, twins show differences in protein expression.13 Therefore, there must
be some interaction between the genes and the environment.
Importantly, not all of the data support chimp-human common ancestry as nicely as
evolutionists typically suggest. In particular, when scientists made a careful
comparison between human, chimpanzee, and gorilla genomes, they found a significant
number of genetic markers where humans matched gorillas more closely than
chimpanzees! Indeed, at 18–29 percent of the genetic markers, either humans and
gorillas or chimpanzees and gorillas had a closer match to each other than
chimpanzees and humans.14
These results are certainly not what one would expect according to standard
evolutionary theory. Chimpanzees and humans are supposed to share a more recent
common ancestor with each other than either have with the gorilla. Trying to
account for the unexpected distribution of common markers that would otherwise
conflict with evolutionary predictions, the authors of this study made the bizarre
suggestion: Perhaps chimpanzees and humans split off from a common ancestor, but
later descendants of each reproduced to form chimp-human hybrids. Such an
“explanation” appears to be an attempt to rescue the concept of chimp-human common
ancestry rather than to provide the data to confirm this hypothesis.
All Similarities Are Not Equal
Many genetic defects are the result of a single change in an amino acid.
A high degree of sequence similarity does not equate to proteins having exactly the
same function or role. For example, the FOXP2 protein, which has been shown to be
involved in language, has only 2 out of about 700 amino acids which are different
between chimpanzees and humans.15 This means they are 99.7 percent identical. While
this might seem like a trivial difference, consider exactly what those differences
are. In the FOXP2 protein, humans have the amino acid asparagine instead of
threonine at position 303 and then a serine that is in place of an asparagine at
325. Although apparently a minor alteration, the second change can make a
significant difference in the way the protein functions and is regulated.16 Thus, a
very high degree of sequence similarity can be irrelevant if the amino acid that is
different plays a crucial role. Indeed, many genetic defects are the result of a
single change in an amino acid. For example, sickle cell anemia results from a
valine replacing glutamic acid in the hemoglobin protein. It does not matter that
every other amino acid is exactly the same.
Usually people think that differences in amino acid sequence only alter the three-
dimensional shape of a protein. FOXP2 demonstrates how a difference in one amino
acid can yield a protein that is regulated differently or has altered functions.
Therefore, we should not be too quick to trivialize even very small differences in
gene sequences. Further, slight differences in regions that don’t code for proteins
can impact how protein levels are regulated. This alteration can change the amount
of protein that is produced or when it is produced. In such cases, the high degree
of similarity is meaningless because of the significant functional differences that
result from altered protein levels.
What about Similar “Junk DNA” in Human and Chimp DNA?
Evolutionists have suggested that there are “plagiarized mistakes” between the
human and chimpanzee genome and that these are best explained by a common ancestor.
A teacher who found identical errors on two students’ papers would be rightly
inclined to believe that the students cheated. The best explanation for two papers
with an identical error is that they are both from the same original source. In the
same way, some evolutionists have suggested that differences or deactivated genes
shared by humans and chimps are best explained by common ancestry. They claim that
the only alternative is a Creator who put the same error in two different organisms
—a claim they would call incredible.
Evolutionists may consider something to be an error when there is a perfectly good
reason that is yet unexplained. They conclude that the error is the result of an
ancient mutation based on evolutionary assumptions. Further, when it comes to DNA,
there may be genetic hotspots that are prone to the same mutation. For example,
humans and guinea pigs share alleged mistakes in the vitamin C pseudogene without
sharing a recent common ancestor.17
Examples of the alleged “plagiarized mistakes” are endogenous retroviruses (ERVs)—
part of the so-called “junk DNA.” ERVs are stretches of DNA that can be spliced
(cut out), copied, and inserted into other locations within the genome. There are
many different types of these mobile pieces of DNA.18
The ERVs are not always consistent with evolutionary expectations. For example,
scientists analyzed the complement component C4 genes (an aspect of the immune
system) in a variety of primates.19 Both chimpanzees and gorillas had short C4
genes. The human gene was long because of an ERV. Interestingly, orangutans and
green monkeys had the same ERV inserted at exactly the same point. This is
especially significant because humans are supposed to have a more recent common
ancestor with both chimpanzees and gorillas and only more distantly with
orangutans. Yet the same ERV in exactly the same position would imply that humans
and orangutans had the more recent common ancestor. Here is a good case where ERVs
do not line up with the expected evolutionary progression. Nonetheless, they are
still held up as evidence for common ancestry.
Additional evidence has suggested that ERVs may in fact have functions.20 One very
important function has to do with implantation during pregnancy.21
What about the Alleged Fusion of Human Chromosome 2?
Humans normally have 23 pairs of chromosomes while chimpanzees have 24.
Evolutionary scientists believe that human chromosome 2 has been formed through the
fusion of two small chromosomes in an ape-like ancestor in the human lineage
instead of an intrinsic difference resulting from a separate creation. While this
may account for the difference in chromosome number, a clear and practical
mechanism for how a chromosomal abnormality becomes universal in such a large
population is lacking. The fusion would have occurred once in a single individual.
Every single human being on earth would have to be a descendant of that one
individual. Because there is no selective advantage to a fused chromosome, this
becomes even more difficult for evolutionists to explain since natural selection
would not be a factor.
Evolution proponents who insist that the chromosome 2 fusion event proves that
humans and chimpanzees shared a common ancestor are employing a logical fallacy
known as affirming the consequent. Affirming the consequent follows the pattern:
If P, then Q
Q
Therefore, P
In other words,
If humans and chimpanzees share a common ancestor, then there will be evidence of
chromosome fusion.
There is evidence of chromosome fusion.
Therefore, humans and chimpanzees share a common ancestor.
Here is why it is a logical fallacy: For the sake of the argument, let us assume
that humans are descended from ancestors that had 48 chromosomes just like the
apes, and that there was a common ancestor five million years ago. The alleged
chromosome 2 fusion would have occurred after the human line split from that of
chimpanzees and been passed to all humans on the planet. Even in an evolutionary
scenario, the chromosome fusion does not provide evidence for continuity between
humans and chimps because it only links those individuals that share the fusion.22
In other words, there is no extra evidence for humans having an ancestor in common
with chimpanzees provided by the fusion of chromosome 2. It is no more compelling
than it would be if humans and chimpanzees had the same number—48. One could even
argue that common ancestry with chimpanzees is less compelling because of the
alleged fusion on chromosome 2.
Conclusion
The similarity between human and chimpanzee DNA is really in the eye of the
beholder. If you look for similarities, you can find them. But if you look for
differences, you can find those as well. There are significant differences between
the human and chimpanzee genomes that are not easily accounted for in an
evolutionary scenario.
Creationists expect both similarities and differences, and that is exactly what we
find. The fact that many humans, chimps, and other creatures share genes should be
no surprise to the Christian. The differences are significant. Many in the
evolutionary world like to discuss the similarities while brushing the differences
aside. Emphasis on percent DNA similarity misses the point because it ignores both
the magnitude of the actual differences as well as the significance of the role
that single amino acid changes can play.
Please consider the implications of the worldviews that are in conflict regarding
the origin of mankind. The Bible teaches that man was uniquely formed and made in
the image of God (Genesis 1 and 2). The Lord directly fashioned the first man Adam
from dust and the first woman Eve from Adam’s side. He was intimately involved from
the beginning and is still intimately involved. Keep in mind that the Lord Jesus
Christ stepped into history to become a man—not a chimp—and now offers the free
gift of salvation to those who receive Him.
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Footnotes
1. For example, D.E. Wildman et al., “Implications of Natural Selection in Shaping
99.4% Nonsynonymous DNA Identity between Humans and Chimpanzees: Enlarging Genus
Homo,” Proc. Natl. Acad. Sci. 100 no. 12 (2003): 7181–7188.
2. The Chimpanzee Sequencing and Analysis Consortium 2005, “Initial Sequence of the
Chimpanzee Genome and Comparison with the Human Genome,” Nature 437 (2005): 69–87.
3. Alan Boyle, “Chimp Genetic Code Opens Human Frontiers,” MSNBC,
www.msnbc.msn.com/id/9136200.
4. The Medical News, “Charles Darwin Was Right and Chimp Gene Map Proves It,”
www.news-medical.net/news/2005/08/31/12840.aspx.
5. Studies of chimp-human similarity have typically ignored insertions and
deletions although these account for most of the differences. A study by Roy
Britten included these insertions and deletions and obtained a figure that is close
to the 4 percent reported for the full sequence. See Roy J. Britten, “Divergence
Between Samples of Chimpanzee and Human DNA Sequence Is 5% Counting Indels,” Proc.
Nat. Acad. Sci. 99 no. 21 (2002): 13633–13635.
6. Individuals within a population are variable and some chimps will have more or
fewer nucleotide differences with humans. This variation accounts for a portion of
the differences. 1.06 percent are believed to be fixed differences. Fixed
differences represent those that are universal. In other words, all chimpanzees
have a given nucleotide and all humans have a different one at the same position.
7. Walter J. ReMine, “Cost Theory and the Cost of Substitution—A Clarification,” TJ
19 no. 1 (2005): 113–125. Note also: This problem is exacerbated because most of
the differences between the two organisms are likely due to neutral or random
genetic drift. That refers to change in which natural selection is not operating.
Without a selective advantage, it is difficult to explain how this huge number of
mutations could become fixed in both populations. Instead, many of these may
actually be intrinsic sequence differences present from the beginning of creation.
8. Discussed in D.A. DeWitt, “Greater than 98% Chimp/Human DNA Similarity? Not Any
More,” TJ 17 no. 1 (2003): 8–10.
9. S. Kakuo, K. Asaoka, and T. Ide, “Human Is a Unique Species Among Primates in
Terms of Telomere Length,” Biochem. Biophys. Res. Commun. 263 (1999): 308–314.
10. Ann Gibbons, “Which of Our Genes Make Us Human?” Science 281 (1998): 1432–1434.
11. Y. Gilad et al., “Expression Profiling in Primates Reveals a Rapid Evolution of
Human Transcription Factors,” Nature 440 (2006): 242–245.
12. J.P. Demuth et al., “The Evolution of Mammalian Gene Families,” PLoS ONE 1 no.
1 (2006): e85, www.plosone.org/article/info:doi%2F10.1371%2Fjournal.pone.0000085.
13. M.F. Fraga et al., “Epigenetic Differences Arise During the Lifetime of
Monozygotic Twins,” Proc. Natl. Acad. Sci. 102 no. 30 (2005): 10,604–10,609.
14. N. Patterson et al., “Genetic Evidence for Complex Speciation of Humans and
Chimpanzees,” Nature 441 (2006): 315–321.
15. W. Enard et al., “Molecular Evolution of FOXP2, a Gene Involved in Speech and
Language,” Nature 418 (2002): 869–872.
16. This difference in amino acid sequence opens up a potential phosphorylation
site for protein kinase C. Phosphorylation is a major mechanism for regulating the
activity of enzymes as well as transcription factors.
17. Y. Inai, Y. Ohta, and M. Nishikimi, “The Whole Structure of the Human
Nonfunctional L-Gulono-Gamma-Lactone Oxidase Gene—the Gene Responsible for Scurvy—
and the Evolution of Repetitive Sequences Theron,” J Nutr Sci Vitimol 49 (2003):
315–319.
18. Humans have many more short interspersed elements (SINEs) than chimps, but
chimps have two novel families of retroviral elements, which are absent from man.
Comparing endogenous “retroviral elements” yielded 73 human-specific insertions and
45 chimpanzee-specific insertions. Humans have two SINE (Alu) families that the
chimpanzees lack and humans have significantly more copies (approximately 7,000
human-specific copies versus approx. 2,300 chimpanzee-specific ones). There are
also approximately 2,000 lineage specific L1 elements. All of these lineage
specific changes would be required to take place sometime between the last
chimp/human common ancestor and the most recent common ancestor for all people on
the planet. Importantly, these are modifications for which there is no known
selective advantage.
19. A.W. Dangel et al., “Complement Component C4 Gene Intron 9 Has a Phylogenetic
Marker for Primates: Long Terminal Repeats of the Endogenous Retrovirus ERV-K(C4)
Are a Molecular Clock of Evolution,” Immunogenetics 42 no. 1 (1995): 41–52.
20. Georgia Purdom, “Human Endogenous Retroviruses (HERVs)—Evolutionary “Junk” or
God’s Tools?” www.answersingenesis.org/docs2006/1219herv.asp.
21. K.A. Dunlap et al., “Endogneous Retroviruses Regulate Periimplantation
Placental Growth and Differentiation,” Proc. Nat. Acad. Sci. 103 no. 29 (2006):
14,390–14,395.
22. There is debate among creationists as to whether the evidence for a chromosome
2 fusion event in humans is compelling. Some believe it is an intrinsic difference;
others are open to it occurring early in human history, perhaps shortly before
Noah. In both cases, evidence linking humans to chimpanzees based on chromosome
fusion is lacking.
Chimp-Human DNA Similarity: What Does It Really Mean?
News to Know
by Dr. Elizabeth Mitchell on June 3, 2013
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Does genomic information show scientifically that Adam is not our collective
ancestor?
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* World: “Adam VersusCclaims from Genetics”
Claims that chimpanzee and human DNA are 96 to 99% identical are used by
evolutionists as “proof” that chimps and humans are descended from a common ape-
like ancestor. The Human Genome Project—according to the interpretations of
evolutionists—scientifically disproved the possibility of all humans being
descended from one man and one woman. But what does the science really demonstrate?
Westminster Theological Journal recently published an informative essay by
Westminster Theological Seminary professor Vern Poythress, who has a Th.D. as well
as a Harvard Ph.D. in mathematics, refuting these claims.
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The statistical similarity between chimp and human DNA relates primarily to the
portions of DNA that code for proteins, ignoring the vast amount of DNA that has
been commonly called “junk DNA,” sections that now appear to have regulatory and
other functions. Furthermore, understanding how DNA is compared reveals the chimp-
human similarity is not all it seems. DNA consists of millions of “bases”—four
kinds of molecules that act like the letters in a code. But contrary to the
impression given in television programs, sequencing DNA is not a matter of simply
lining up long strings with millions of bases to see what matches.
sequence1
The letters in this short sequence symbolizing a bit of DNA code stand for the
bases: guanine, cytosine, adenine, and thymine. The sequence of such bases encode
not only the instructions for the manufacture of all the proteins in a living
organisms but the instructions regulating the use of those proteins and much more.
Some sections of DNA strands being compared match like this, often because the same
sorts of protein molecules are needed in living organisms. Because DNA consists of
millions of bases, sequencing technology breaks it into short segments for
comparison and then much match up the pieces to be compared, effectively ignoring
the segments that differ greatly. Image by Westminster Theological Journal through
World
As a result of technological limitations, comparisons between chimp and human DNA
focus on areas that are similar. Thus, as Dr. Poythress explains, chimp and human
DNA only appear “99%” identical if:
1. repeated sequences are ignored
2. only sections that “align naturally” are compared,
3. and the only differences noted are single base-pair substitutions.
Thus, extra sequences of DNA—commonly called “insertions” and “deletions”—are
ignored. When they are included among the differences, the figure becomes “96%.”
Note that even these names—insertions and deletions—imply an assumption of
evolutionary modifications by which the DNA of a common ancestor was gradually
modified over time. But the science cannot look back to the genome of an imagined
evolutionary ancestor. And a great deal of DNA, when chimps and humans are
compared, simply does not correspond at all and is therefore completely absent from
the oft-quoted statistics. Furthermore, despite evolutionary insistence that the
chimp is our closest relative, gorilla and orangutan DNA is more similar to ours
than chimpanzee is.
Furthermore, though not covered in Poythress’s essay, when the DNA sequences are
compared more objectively without pre-selecting sequences and filtering the data,
the chimp and human genomes are only about 70% similar.
Even more important than an awareness of the limitations on the statistical
similarity between chimp and human DNA is the ability to understand how
evolutionists interpret what genetic similarity there actually is. Biblical
creationists understand that this is a consequence of having a common Designer who
wisely designed humans and animals to function on earth. Poythress explains:
The most striking genetic similarities between humans and chimps lie in many of the
protein coding regions within the DNA. That is understandable from the standpoint
of design, because proteins are the backbone of chemical machinery inside a cell.
Cells have to have machinery for metabolism, for cell division, for translating DNA
into proteins, for dealing with toxins, and for responding to the environment. The
machinery has to accomplish many of the same things in cells of many kinds, so it
should not be surprising that there are similarities among proteins not only
between man and chimpanzee but throughout the world of living things.
The notion that genetic similarities prove shared evolutionary ancestry is a
consequence of naturalistic Darwinian assumptions superimposed on the data.
Evolutionists assume chimps and humans share an evolutionary ancestry and interpret
all data according to that assumption.
sequence2
When sequences being compared differ by only a different base here and there, those
variations are called “substitutions.” Image by Westminster Theological Journal
through World.
sequence3
When one stretch of the DNA being compared contains a sequence absent from the
other, the difference is called an indel, meaning “insertion-deletion.” Implicit in
the terminology is the assumption that the DNA of each diverged from a common
ancestral form. Image by Westminster Theological Journal through World.
As Poythress says, “Darwinism says that all kinds of living things came into being
by purely gradualistic processes. In the popular mind, and indeed also among many
scientists, Darwinism also involves the additional assumption that the process of
change over time was unguided and purposeless—in other words, God, if He exists, is
absent.”
Yet nothing about the science can confirm that God did not act to create humans and
animals as Genesis chapter one reports, without evolution. And nothing about the
science can demonstrate the evolutionary claim that the origin of life was blindly
naturalistic and purposeless. Poythress explains, “That claim overreaches the
evidence and the competence of science. It is really a philosophical and religious
claim.” Thus, atheism is a sort of “religion.”
Evolutionists assert that population genetics and molecular clocks cannot possibly
point back to just two original people 6,000 years ago. Poythress points out that
the calculations which this claim is based on assume that the human genome has
always had constant rates of mutation and recombination. Population studies further
depend on assumptions about the average lifespans of people. Yet Scripture
indicates that lifespans changed dramatically after the global Flood. The notion
that humanity could not have originated with two created people is rooted in
unverifiable assumptions imposed upon the science.
Given the effects of sin’s curse on humanity, the dramatic changes in lifespan over
a few thousand years, and the population bottleneck that occurred when the global
Flood reduced the genomic variety in the human population to those genes in the
eight people on the Ark, the uniformitarian assumptions on which evolutionary
anthropologists and geneticists base their conclusions that the human population
could not have been traced back to Adam and Eve are faulty.
Thus the science in no way “proves” human ancestry from an ape-like ancestor or the
impossibility of human ancestry from Adam and Eve. As to the age of the earth,
while Poythress writes nothing in his essay to suggest millions of years, in his
opinion, the small variations (“gaps”) in the genealogical lists in the Old and New
Testaments make it impossible to know how long ago God created man. However, a
comparison of genealogical lists reveals that, while there are a few places where
God chose to include and exclude certain people, only some genealogies contain
information about time. And those lists, from which we (and Archbishop Ussher)
derive calculations about the timeline of history, consist of numerically
interlocked data rendering the inclusion or exclusion of a particular person—as far
as the timeline goes—irrelevant. As Dr. Floyd Nolen Jones explains in Chronology of
the Old Testament:
The Scripture precisely lists the age of each patriarch (i.e. Arphaxad = 35 years
old) when the next patriarch (i.e. Salah) is born. Thus, even if the next patriarch
in the recorded genealogy was a great-grandson rather than a son, this procedure of
giving the age of one patriarch when the next is born fixes the two men’s lives
relative to each other. In so doing, it provides an exact continuous chronology
across this time span.1
The father’s (ancestor’s) name is mathematically interlocked to the chosen
descendant; hence no gap of time or generation is possible.2
Furthermore, Jude 14 corroborates the Old Testament genealogies, informing us that
Enoch was a member of the seventh generation from Adam. Scripture does not
contradict itself. Biblical history therefore does reveal that God created Adam and
Eve about 6,000 years ago. And the scientific evidence of hominid fossils, genomic
analysis, and population studies only appear to “prove” evolution if the data are
interpreted expressly by presuming evolution happened. Such reasoning is circular.
Science does not disprove Scripture.
A Simple Answer
by Peter Galling on September 19, 2008
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Can a simple “yes or no” answer be adequate for a question about Adam and Eve’s
genetic code and today’s human traits?
I have a question about Adam and Eve. If all human beings are descended from Adam
and Eve, then could we expect to find the code for all human genetic traits in
Adam’s and Eve’s DNA since traits are passed from generation to generation via DNA?
Plaese, a simple "Yes" or "NO". As a believer,I tire of your all to frequent verbal
gymnastics.
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—J., U.S.
If you want a simple yes or no, then no.
Passing the Message
I [had] the privilege of hearing Mr. Carl Kerby speak at my church (First Baptist
Church Seminole, Oklahoma). He was very informative and opened my eyes to a lot of
very useful information. I am sorry that I didn’t get to thank him for his
testimony and his sincere affection for the topics he shared with us. Please pass
this along to him. I will be looking for future events in our region to attend—and
share with others.
—R.R., U.S.
Have Something to Add?
Let us know what you think.
Now that’s the simple answer, and if that’s all you want, J., you don’t need to
read further. However, in some ways “maybe” is a more appropriate answer. We’ve
provided a complete explanation below because explaining our answer to this
question isn’t as simple—some answers just aren’t! So for the logic behind that
answer (we’ll try to avoid verbal gymnastics, though), please read on.
First, a quick overview: the human genetic code is what programs every cell in our
body to do what it does—and thus what gives us many of the physical traits we
exhibit.
In the reproductive process, a sperm cell and an egg cell each contribute 23
chromosomes (made up of DNA) to create a single zygote with 46 chromosomes; these
compose the new map for the developing embryo to follow. Thus, our chromosomes
originate from our parents, who got their genetic information from their parents,
who got it from their parents, who got it from their parents, and so on. Likewise,
we pass on our genetic information to our children, who will pass it to their
children, etc.
Based on the biblical blueprint that we are all descendants of one man and one
woman—Adam (see Acts 17:26 (NIV)) and Eve (see Genesis 3:20)—it would seem
reasonable, then, to conclude that the genetic information in all humans today
ultimately came from Adam and Eve. After all, the only other source would be if God
had created humans again sometime (i.e., separately from Adam and Eve), humans
whose offspring later intermarried with the offspring of Adam and Eve. But the
Bible clearly teaches that this is not the case, as referenced above.1
Now, this would seem to indicate our answer to your question would be a simple yes—
so why did we answer no?
The problem is that, due to the Fall, our bodies don’t always do a perfect job
replicating our genetic information. Instead, there are times when mistakes—
mutations, that is—creep in accidentally. Mutations can be caused by other factors,
too, such as certain types of radiation. Some of these mutations occur in our
somatic cells (e.g., skin cells), and thus, they are never passed along to any
offspring. But if the mutation occurs in a germ cell (i.e., either a sperm or egg
cell) that then fertilizes or becomes fertilized, the mutation will affect the
offspring instead. This is called a germline mutation.
Mutations that result in new characteristics (traits) that weren’t present in the
parent individual are thus “new” genetic traits. The traits would not have been
present in Adam and Eve, but instead arose through mutations along the way;
however, it’s important to note that they are not new genetic information (which
I’ll explain in a moment).
Various factors influence whether the outcome of these mutations is beneficial,
neutral, or harmful. Most are harmful—for example, the many forms of mental
retardation that have hereditary elements; cystic fibrosis; Tay-Sachs; albinism;2
and many other traits (though we would call most “disorders”).
Some traits would be considered relatively neutral. For example, red hair is often
the result of mutations (see How we got red hair (it wasn’t by evolution)); this
would generally be considered neither beneficial nor harmful, though it does
increase the risk of skin cancer (but much less than albinism). Likewise, while
having six fingers on each hand may make it harder to find a pair of gloves that
fit, it is, relatively speaking, a fairly neutral result of mutation-caused genetic
abnormality.
Some mutations may have beneficial outcomes under certain circumstances (note that
this is not through the addition of new information), though they also have
detrimental aspects as well. For example, sickle-cell trait confers reduced
susceptibility to malaria. However, those with this disorder are more likely to
suffer severe problems and even death under other circumstances, such as great
physical exertion, dehydration, and high altitudes, among other deleterious
effects.
But whether the traits these mutations have caused are beneficial, neutral, or
harmful, none of them would have been present in God’s original perfect creation.3
They are all, instead, a result of the Fall, in which Adam’s sin led to corruption
in our world—and in our genetic mechanisms.
But now we get into the confusing world of semantics. We’ve explained that some
genetic traits originated after the Fall, and thus those traits were not present in
Adam and Eve’s DNA, instead having arisen through mutations. However, lest we
confuse any readers, we’re definitely not saying that any new information has been
added to the human genome, and it’s in saying this that we get into some tricky
semantics. How can there be new genetic traits without new information? We’ll use a
brief analogy to explain.
Let’s say I send a short “chain text message” to a friend of mine. The message is
simply “Jan may have just won ten million dollars worth of Zippy Cola! Pass it on!”
Trying to conserve manual exertion as my friend relays the message to his parents
via computer, he types out, “Jan may have just won ten million dollars worth of
Zippy Cola!” They spread the word, and as it spreads on and on, the sentence begins
to change:
* “Jan may have just won ten million dollars worth of Zippy Cola!”
* “Jan may have won ten million dollars worth of Zippy Cola!”
* “Jan may have won ten million dollars wroth of cola!”
* “Jan may have won ten million dollars wroth of cola dollars wroth of cola!”
* “Jan may have won ten million dollars!”
* “Jan m ayhave won ten million dollars!”
* “Jan won ten million dollars!”
* “Jan won ten miloon dollars!”
* “Jan won ten dollars!”
Each sentence is like a different trait in that the ultimate “meaning” is
different. For example, just as the original sentence conveys a very different idea
than the final variation, so the genes coding for brown hair likewise cause the
body to do something different than genes coding for red hair.
However, notice that no new information has been added in our sentence example; all
the information present in the last variation was in the original, even though they
mean different things. There’s also some meaningless junk accumulated along the
way.
So was the mutation that causes cystic fibrosis in Adam and Eve? No. But the gene
that ultimately became mutated (after the Fall) and now causes cystic fibrosis was
present (in Adam and Eve before the Fall). So, in a way the answer to your question
is both “yes” and “no.” And that’s why we would ideally answer “maybe.”
The key points to remember are that, first, we are in no way more physically human
now than we were at creation; second, the human genome has devolved through
mutations and time, such that there is less genetic information, not more; and
third, while not all of the traits present today were present in the Garden of
Eden, they originated sometime after the Curse allowed corruption to creep into our
genome.
gymnastics.
As I’ve described above, the answer is definitely not a simple one. I can’t help
but wonder why you specifically asked us for a simple yes or no and accused us of
“verbal gymnastics.” It is true that sometimes the technical science or philosophy
we write about requires a more complicated response, and we certainly apologize if
you found any of our articles unclear or poorly worded, but by no means do we
attempt to confuse or deceive readers. Rather, we attempt to “demolish arguments
and every pretension that sets itself up against the knowledge of God, and we take
captive every thought to make it obedient to Christ” (2 Corinthians 10:5).
If you do believe that any of our articles have confusing or deceptive passages,
please let us know, and perhaps we can clarify or point you to a better article. A
great place for anyone interested in biblical creation to start is the New Answers
Book, which covers many of the most frequently asked questions we receive.
One final thought: where we succeed in communicating well in our writings,
presentations, and other products, it is a credit to God and His revelation, and
where we fail it is because of our own shortcomings. Perhaps we have articles that
aren’t clear; certainly we have ideas that may ultimately be shown to be incorrect,
although their basis, the Bible, is infallible. Yet insofar as we preach God’s Word
and point people back to the Bible (and God) as the source of ultimate truth, we
have no apologies.
In Christ,
Peter Galling, AiG–U.S.
Footnotes
1. Of course, one could also hypothesize other wild ideas, such as the possibility
of DNA from Nephilim entering the human race—see Nephilim: Who Were They? for a
good analysis.
2. Albinism is considered harmful because of the greater likelihood of skin cancer
and related photophobia.
3. This goes for animals as well. Flightless beetles, polydactyl cats, blind cave
fish, and poodles wouldn’t have been around in Eden, but instead have arisen
through genetic mutations (sometimes with the help of natural selection) since
then.
Chapter 10
What About the Similarity Between Human and Chimp DNA?
by Dr. David A. DeWitt on January 14, 2014
Featured in The New Answers Book 3
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DNA similarity could easily be explained as a result of a common Creator.
The first thing I want to do is clear up a common misconception—especially among
many within the Church. Many falsely believe that in an evolutionary worldview
humans evolved from chimpanzees. And so they ask, “If humans came from chimps, then
why are there still chimps?” However, this is not a good question to ask because an
evolutionary worldview does not teach this. The evolutionists commonly teach that
humans and chimpanzees are both basically “cousins” and have a common ancestor in
our past. If you go back far enough, all life likely has a single common ancestor
in the evolutionary view. This, of course, does not mesh with Genesis 1–2.
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Evolutionists frequently assert that the similarity in DNA sequences provides
evidence that all organisms (especially humans and chimps) are descended from a
common ancestor. However, DNA similarity could just as easily be explained as the
result of a common Creator.
Human designers frequently reuse the same elements and features, albeit with
modifications. Since all living things share the same world, it should be expected
that there would be similarities in DNA as the organisms would have similar needs.
Indeed, it would be quite surprising if every living thing had completely different
sequences for each protein—especially ones that carried out the same function.
Organisms that have highly similar functionality and physiological needs would be
expected to have a degree of DNA similarity.
What Is DNA?
DNA
Figure 1. The double-stranded DNA molecule forms with an A opposite a T and a G

opposite a C. This sequence determines the structure of proteins.
Every living cell contains DNA (deoxyribonucleic acid), which provides the
hereditary instructions for living things to survive, grow, and reproduce. The DNA
is comprised of chemicals called bases, which are paired and put together in
double-stranded chains. There are four different bases, which are represented by
the letters A, T, C, and G. Because A is always paired with T and C is always
paired with G, one strand of DNA can serve as a template for producing the other
strand.
The DNA is transcribed into a single chain of nucleotides called RNA (ribonucleic
acid), which is then translated into the amino acid sequence of a protein. In this
way, the sequence of bases in DNA determines the sequence of amino acids in a
protein which in turn determines the protein structure and function.
In the human genome (total genetic information in the nucleus of the cell), there
are roughly three billion base pairs of DNA with about 20,000 genes (regions that
code for proteins). Surprisingly, only about 1 percent of the DNA actually codes
for proteins. The rest is non-coding DNA. Some of this DNA comprises control areas—
segments of DNA responsible for turning genes on and off, controlling the amount
and timing of protein production. There are also portions of DNA that play
structural roles. Still other regions of DNA have as yet unknown functions.
What Is the Real Percent Similarity between Humans and Chimpanzees?
Apes
Figures 2 and 3: Evolutionists believe that the similarity in the DNA sequence of
gorillas, chimpanzees, and humans is proof that they all share a common ancestor
(Photos: Shutterstock)
(physical/visible) similarities between humans and the great apes, including
chimpanzees, gorillas, and orangutans. Over the last few decades, molecular
biologists have joined the fray, pointing out the similarities in DNA sequences.
Previous estimates of genetic similarity between humans and chimpanzees suggested
they were 98.5–99.4 percent identical.1
Because of this similarity, evolutionists have viewed the chimpanzee as “our
closest living relative.” Most early comparative studies were carried out only on
genes (such as the sequence of the cytochrome c protein), which constituted only a
very tiny fraction of the roughly three billion DNA base pairs that comprise our
genetic blueprint. Although the full human genome sequence has been available since
2001, the whole chimpanzee genome has not. Thus, much of the previous work was
based on only a fraction of the total DNA.
Nature magazine
Figure 4: The journal Nature often trumpets the common ancestry of humans and
chimps.
In the fall of 2005, in a special issue of Nature devoted to chimpanzees,
researchers reported the draft sequence of the chimpanzee genome.2 At the time,
some researchers called it “the most dramatic confirmation yet”3 of Darwin’s theory
that man shared a common ancestor with the apes. One headline read: “Charles Darwin
Was Right and Chimp Gene Map Proves It.”4
Researchers found 96 percent genetic similarity and a difference between us of 4
percent. This is a very strange kind of proof because it is actually double the
percent difference that evolutionists have claimed for years!5 Even so, no matter
what the actual percent difference turned out to be, whether 2, 4, or 10 percent,
they still would have claimed that Darwin was right to support their worldview.
example, 1.23 percent of the differences are single base pair substitutions (figure
5).6 This doesn’t sound like much until you realize that it represents about 35
million differences! But that is only the beginning. There are 40–45 million bases
present in humans that are missing from chimps and about the same number present in
chimps that are absent from man. These extra DNA nucleotides are called
“insertions” or “deletions” because they are thought to have been added to or lost
from the original sequence. (Substitutions and insertions are compared in figure
5.) This puts the total number of DNA differences at about 125 million. However,
since the insertions can be more than one nucleotide long, there are about 40
million total separate mutation events that would separate the two species in the
evolutionary view.
DNA Comparison
Figure 5: Comparison between a base substitution and an insertion/deletion. Two DNA

sequences can be compared. If there is a difference in the nucleotides (e.g., an A
instead of a G) at a given position, this is a substitution. In contrast, if there
is a nucleotide base that is missing it is considered an insertion/deletion. It is
assumed that a nucleotide has been inserted into one of the sequences or one has
been deleted from the other. It is often too difficult to determine whether the
difference is a result of an insertion or a deletion and thus it is called an
“indel.” Indels can be of virtually any length.
To put this number into perspective, a typical 8½ x 11-inch page of text might have
4,000 letters and spaces. It would take 10,000 such pages full of text to equal 40
million letters! So the difference between humans and chimpanzees includes about 35
million DNA bases that are different, about 45 million in the human that are absent
from the chimp, and about 45 million in the chimp that are absent from the human.
the Bible says in Genesis 2. Therefore, man and the apes have never had an ancestor
in common. Assuming they did, for the sake of analyzing the argument, then 40
million separate mutation events would have had to take place and become fixed in
the population in only 300,000 generations. This is an average of 133 mutations
locked into the genome every generation. Locking in such a staggering number of
mutations in a relatively small number of generations is a problem referred to as
“Haldane’s dilemma.”7
There are many other differences between chimpanzee and human genomes that are not
quantifiable as percentages.8 Specific examples of these differences include:
At the end of each chromosome is a string of repeating DNA sequences called
telomeres. Chimpanzees and other apes have about 23,000 base pairs of DNA at their
telomeres. Humans are unique among primates with much shorter telomeres only 10,000
long.9
While 18 pairs of chromosomes are virtually identical, chromosomes 4, 9, and 12
show evidence of being “remodeled.”10 In other words, the genes and markers on
these chromosomes are not in the same order in the human and chimpanzee. Instead of
being “remodeled,” as the evolutionists suggest, these could also be intrinsic
differences as each was a separate creation.
Even with genetic similarity, there can be differences in the amount of specific
proteins produced. Just because DNA sequences are similar does not mean that the
same amounts of the proteins are produced. Such differences in protein expression
can yield vastly different responses in cells. Roughly 10 percent of genes examined
showed significant differences in expression levels between chimpanzees and
humans.11
Gene families are groups of genes that have similar sequences and also similar
functions. Scientists comparing the number of genes in gene families have revealed
significant differences between humans and chimpanzees. Humans have 689 genes that
chimps lack and chimps have 86 genes that humans lack. Such differences mean that 6
percent of the gene complement is different between humans and chimpanzees,
irrespective of the individual DNA base pairs.12
Thus, the percentage of matching DNA is only one measure of how similar two
organisms are, and not really a good one at that. There are other factors besides
DNA sequence that determine an organism’s phenotype (how traits are physically
expressed). Indeed, even though identical twins have the same DNA sequence, as they
grow older, twins show differences in protein expression.13 Therefore, there must
be some interaction between the genes and the environment.
Importantly, not all of the data support chimp-human common ancestry as nicely as
evolutionists typically suggest. In particular, when scientists made a careful
comparison between human, chimpanzee, and gorilla genomes, they found a significant
number of genetic markers where humans matched gorillas more closely than
chimpanzees! Indeed, at 18–29 percent of the genetic markers, either humans and
gorillas or chimpanzees and gorillas had a closer match to each other than
chimpanzees and humans.14
These results are certainly not what one would expect according to standard
evolutionary theory. Chimpanzees and humans are supposed to share a more recent
common ancestor with each other than either have with the gorilla. Trying to
account for the unexpected distribution of common markers that would otherwise
conflict with evolutionary predictions, the authors of this study made the bizarre
suggestion: Perhaps chimpanzees and humans split off from a common ancestor, but
later descendants of each reproduced to form chimp-human hybrids. Such an
“explanation” appears to be an attempt to rescue the concept of chimp-human common
ancestry rather than to provide the data to confirm this hypothesis.
All Similarities Are Not Equal
Many genetic defects are the result of a single change in an amino acid.
A high degree of sequence similarity does not equate to proteins having exactly the
same function or role. For example, the FOXP2 protein, which has been shown to be
involved in language, has only 2 out of about 700 amino acids which are different
between chimpanzees and humans.15 This means they are 99.7 percent identical. While
this might seem like a trivial difference, consider exactly what those differences
are. In the FOXP2 protein, humans have the amino acid asparagine instead of
threonine at position 303 and then a serine that is in place of an asparagine at
325. Although apparently a minor alteration, the second change can make a
significant difference in the way the protein functions and is regulated.16 Thus, a
very high degree of sequence similarity can be irrelevant if the amino acid that is
different plays a crucial role. Indeed, many genetic defects are the result of a
single change in an amino acid. For example, sickle cell anemia results from a
valine replacing glutamic acid in the hemoglobin protein. It does not matter that
every other amino acid is exactly the same.
Usually people think that differences in amino acid sequence only alter the three-
dimensional shape of a protein. FOXP2 demonstrates how a difference in one amino
acid can yield a protein that is regulated differently or has altered functions.
Therefore, we should not be too quick to trivialize even very small differences in
gene sequences. Further, slight differences in regions that don’t code for proteins
can impact how protein levels are regulated. This alteration can change the amount
of protein that is produced or when it is produced. In such cases, the high degree
of similarity is meaningless because of the significant functional differences that
result from altered protein levels.
What about Similar “Junk DNA” in Human and Chimp DNA?
Evolutionists have suggested that there are “plagiarized mistakes” between the
human and chimpanzee genome and that these are best explained by a common ancestor.
A teacher who found identical errors on two students’ papers would be rightly
inclined to believe that the students cheated. The best explanation for two papers
with an identical error is that they are both from the same original source. In the
same way, some evolutionists have suggested that differences or deactivated genes
shared by humans and chimps are best explained by common ancestry. They claim that
the only alternative is a Creator who put the same error in two different organisms
—a claim they would call incredible.
Evolutionists may consider something to be an error when there is a perfectly good
reason that is yet unexplained. They conclude that the error is the result of an
ancient mutation based on evolutionary assumptions. Further, when it comes to DNA,
there may be genetic hotspots that are prone to the same mutation. For example,
humans and guinea pigs share alleged mistakes in the vitamin C pseudogene without
sharing a recent common ancestor.17
Examples of the alleged “plagiarized mistakes” are endogenous retroviruses (ERVs)—
part of the so-called “junk DNA.” ERVs are stretches of DNA that can be spliced
(cut out), copied, and inserted into other locations within the genome. There are
many different types of these mobile pieces of DNA.18
The ERVs are not always consistent with evolutionary expectations. For example,
scientists analyzed the complement component C4 genes (an aspect of the immune
system) in a variety of primates.19 Both chimpanzees and gorillas had short C4
genes. The human gene was long because of an ERV. Interestingly, orangutans and
green monkeys had the same ERV inserted at exactly the same point. This is
especially significant because humans are supposed to have a more recent common
ancestor with both chimpanzees and gorillas and only more distantly with
orangutans. Yet the same ERV in exactly the same position would imply that humans
and orangutans had the more recent common ancestor. Here is a good case where ERVs
do not line up with the expected evolutionary progression. Nonetheless, they are
still held up as evidence for common ancestry.
Additional evidence has suggested that ERVs may in fact have functions.20 One very
important function has to do with implantation during pregnancy.21
What about the Alleged Fusion of Human Chromosome 2?
Humans normally have 23 pairs of chromosomes while chimpanzees have 24.
Evolutionary scientists believe that human chromosome 2 has been formed through the
fusion of two small chromosomes in an ape-like ancestor in the human lineage
instead of an intrinsic difference resulting from a separate creation. While this
may account for the difference in chromosome number, a clear and practical
mechanism for how a chromosomal abnormality becomes universal in such a large
population is lacking. The fusion would have occurred once in a single individual.
Every single human being on earth would have to be a descendant of that one
individual. Because there is no selective advantage to a fused chromosome, this
becomes even more difficult for evolutionists to explain since natural selection
would not be a factor.
Evolution proponents who insist that the chromosome 2 fusion event proves that
humans and chimpanzees shared a common ancestor are employing a logical fallacy
known as affirming the consequent. Affirming the consequent follows the pattern:
If P, then Q
Q
Therefore, P
In other words,
If humans and chimpanzees share a common ancestor, then there will be evidence of
chromosome fusion.
There is evidence of chromosome fusion.
Therefore, humans and chimpanzees share a common ancestor.
Here is why it is a logical fallacy: For the sake of the argument, let us assume
that humans are descended from ancestors that had 48 chromosomes just like the
apes, and that there was a common ancestor five million years ago. The alleged
chromosome 2 fusion would have occurred after the human line split from that of
chimpanzees and been passed to all humans on the planet. Even in an evolutionary
scenario, the chromosome fusion does not provide evidence for continuity between
humans and chimps because it only links those individuals that share the fusion.22
In other words, there is no extra evidence for humans having an ancestor in common
with chimpanzees provided by the fusion of chromosome 2. It is no more compelling
than it would be if humans and chimpanzees had the same number—48. One could even
argue that common ancestry with chimpanzees is less compelling because of the
alleged fusion on chromosome 2.
Conclusion
The similarity between human and chimpanzee DNA is really in the eye of the
beholder. If you look for similarities, you can find them. But if you look for
differences, you can find those as well. There are significant differences between
the human and chimpanzee genomes that are not easily accounted for in an
evolutionary scenario.
Creationists expect both similarities and differences, and that is exactly what we
find. The fact that many humans, chimps, and other creatures share genes should be
no surprise to the Christian. The differences are significant. Many in the
evolutionary world like to discuss the similarities while brushing the differences
aside. Emphasis on percent DNA similarity misses the point because it ignores both
the magnitude of the actual differences as well as the significance of the role
that single amino acid changes can play.
Please consider the implications of the worldviews that are in conflict regarding
the origin of mankind. The Bible teaches that man was uniquely formed and made in
the image of God (Genesis 1 and 2). The Lord directly fashioned the first man Adam
from dust and the first woman Eve from Adam’s side. He was intimately involved from
the beginning and is still intimately involved. Keep in mind that the Lord Jesus
Christ stepped into history to become a man—not a chimp—and now offers the free
gift of salvation to those who receive Him.
Footnotes
1. For example, D.E. Wildman et al., “Implications of Natural Selection in Shaping
99.4% Nonsynonymous DNA Identity between Humans and Chimpanzees: Enlarging Genus
Homo,” Proc. Natl. Acad. Sci. 100 no. 12 (2003): 7181–7188.
2. The Chimpanzee Sequencing and Analysis Consortium 2005, “Initial Sequence of the
Chimpanzee Genome and Comparison with the Human Genome,” Nature 437 (2005): 69–87.
3. Alan Boyle, “Chimp Genetic Code Opens Human Frontiers,” MSNBC,
www.msnbc.msn.com/id/9136200.
4. The Medical News, “Charles Darwin Was Right and Chimp Gene Map Proves It,”
www.news-medical.net/news/2005/08/31/12840.aspx.
deletions although these account for most of the differences. A study by Roy
to the 4 percent reported for the full sequence. See Roy J. Britten, “Divergence
Between Samples of Chimpanzee and Human DNA Sequence Is 5% Counting Indels,” Proc.
Nat. Acad. Sci. 99 no. 21 (2002): 13633–13635.
6. Individuals within a population are variable and some chimps will have more or
fewer nucleotide differences with humans. This variation accounts for a portion of
the differences. 1.06 percent are believed to be fixed differences. Fixed
differences represent those that are universal. In other words, all chimpanzees
have a given nucleotide and all humans have a different one at the same position.
7. Walter J. ReMine, “Cost Theory and the Cost of Substitution—A Clarification,” TJ
19 no. 1 (2005): 113–125. Note also: This problem is exacerbated because most of
the differences between the two organisms are likely due to neutral or random
genetic drift. That refers to change in which natural selection is not operating.
Without a selective advantage, it is difficult to explain how this huge number of
mutations could become fixed in both populations. Instead, many of these may
actually be intrinsic sequence differences present from the beginning of creation.
8. Discussed in D.A. DeWitt, “Greater than 98% Chimp/Human DNA Similarity? Not Any
More,” TJ 17 no. 1 (2003): 8–10.
9. S. Kakuo, K. Asaoka, and T. Ide, “Human Is a Unique Species Among Primates in
Terms of Telomere Length,” Biochem. Biophys. Res. Commun. 263 (1999): 308–314.
10. Ann Gibbons, “Which of Our Genes Make Us Human?” Science 281 (1998): 1432–1434.
11. Y. Gilad et al., “Expression Profiling in Primates Reveals a Rapid Evolution of
Human Transcription Factors,” Nature 440 (2006): 242–245.
12. J.P. Demuth et al., “The Evolution of Mammalian Gene Families,” PLoS ONE 1 no.
1 (2006): e85, www.plosone.org/article/info:doi%2F10.1371%2Fjournal.pone.0000085.
13. M.F. Fraga et al., “Epigenetic Differences Arise During the Lifetime of
Monozygotic Twins,” Proc. Natl. Acad. Sci. 102 no. 30 (2005): 10,604–10,609.
14. N. Patterson et al., “Genetic Evidence for Complex Speciation of Humans and
Chimpanzees,” Nature 441 (2006): 315–321.
15. W. Enard et al., “Molecular Evolution of FOXP2, a Gene Involved in Speech and
Language,” Nature 418 (2002): 869–872.
16. This difference in amino acid sequence opens up a potential phosphorylation
site for protein kinase C. Phosphorylation is a major mechanism for regulating the
activity of enzymes as well as transcription factors.
17. Y. Inai, Y. Ohta, and M. Nishikimi, “The Whole Structure of the Human
Nonfunctional L-Gulono-Gamma-Lactone Oxidase Gene—the Gene Responsible for Scurvy—
and the Evolution of Repetitive Sequences Theron,” J Nutr Sci Vitimol 49 (2003):
315–319.
18. Humans have many more short interspersed elements (SINEs) than chimps, but
chimps have two novel families of retroviral elements, which are absent from man.
Comparing endogenous “retroviral elements” yielded 73 human-specific insertions and
45 chimpanzee-specific insertions. Humans have two SINE (Alu) families that the
chimpanzees lack and humans have significantly more copies (approximately 7,000
human-specific copies versus approx. 2,300 chimpanzee-specific ones). There are
also approximately 2,000 lineage specific L1 elements. All of these lineage
specific changes would be required to take place sometime between the last
chimp/human common ancestor and the most recent common ancestor for all people on
the planet. Importantly, these are modifications for which there is no known
selective advantage.
19. A.W. Dangel et al., “Complement Component C4 Gene Intron 9 Has a Phylogenetic
Marker for Primates: Long Terminal Repeats of the Endogenous Retrovirus ERV-K(C4)
Are a Molecular Clock of Evolution,” Immunogenetics 42 no. 1 (1995): 41–52.
20. Georgia Purdom, “Human Endogenous Retroviruses (HERVs)—Evolutionary “Junk” or
God’s Tools?” www.answersingenesis.org/docs2006/1219herv.asp.
21. K.A. Dunlap et al., “Endogneous Retroviruses Regulate Periimplantation
Placental Growth and Differentiation,” Proc. Nat. Acad. Sci. 103 no. 29 (2006):
14,390–14,395.
22. There is debate among creationists as to whether the evidence for a chromosome
2 fusion event in humans is compelling. Some believe it is an intrinsic difference;
others are open to it occurring early in human history, perhaps shortly before
Noah. In both cases, evidence linking humans to chimpanzees based on chromosome
fusion is lacking.
Chromosome Tales and the Importance of a Biblical Worldview
by Dr. Jean Lightner on June 18, 2014
Featured in Answers in Depth
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Abstract
Evidence never speaks for itself; it must be interpreted. When it is interpreted in
a particular worldview, it can sound very convincing that the evidence supports
that worldview. This was the case for the proposed chromosomal fusion that
supposedly resulted in human chromosome 2. It was promoted as unequivocal evidence
that humans and apes shared a common ancestor. In a biblical worldview, it is
possible for a chromosome to have resulted from the fusion of two smaller
chromosomes. However, there were details about the story that didn’t make sense.
The biblical worldview provided the motivation to dig deeper. Further investigation
now makes it clear that human chromosome 2 was not derived from a fusion of ape
chromosomes; its structure is consistent with being designed by a wise Creator.
In my lifetime I have seen a number of supposedly powerful arguments for evolution
come and go. Generally, they seem powerful because it is implied there is only one
way to interpret the evidence, and only an evolutionary interpretation is given. I
have found that the biblical worldview is far more robust, and it is only a matter
of time and some research before it is clear that the evidence is better explained
by a biblical model.
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chromosome merge
Human chromosome 2 was said to have been formed by the fusion of two primate
chromosomes that remain separate in chimps. It was supposed to be an end-to-end
(telomere-to-telomere) fusion. Known fusions in mammals are different in that they
occur near at least one centromere region.
A few years ago I wrote about one example of a “compelling” evolutionary argument,
the supposed evidence for a fusion involving human chromosome 2.1 According to Dr.
Ken Miller, this was incredibly powerful evidence of common ancestry between humans
and apes.2 Since apes have 48 chromosomes (24 pairs) and humans have 46 (23
pairs), evolutionists propose that a fusion occurred to account for the difference.
In a YouTube video Dr. Miller showcases the supposed fusion as a prediction of
evolution and boldly states:
What must have happened is that one pair of chromosomes must have gotten fused. So
we should be able to look at our genome and discover that one of our chromosomes
resulted from the fusion of two primate chromosomes. So we should be able to look
around our genome, and you know what? If we don't find it, evolution is wrong - we
don't share a common ancestor.3
Chromosome fusions do occur. The topic is of particular interest to me, so in my
previous article I highlighted a number of assumptions hidden in Dr. Miller’s
argument. Evidence of a fusion would not be an automatic “slam dunk” against
biblical creation. Interestingly, since that article was written, there has been
considerable research done suggesting that there never was a fusion on human
chromosome 2. According to the quote by Dr. Miller above, this would be a “slam
dunk” against evolution.
What Is Really in the Scientific Literature?
First, an investigation into the scientific literature revealed that scientists
didn’t find the proposed fusion location by hunting for sequences that appeared to
be a fusion site, as Dr. Miller had suggested.4 The idea of a fusion on chromosome
2 was suggested based on the assumption of common ancestry and some similarities
between chimp chromosomes 12 and 13 (now 2A and 2B) and human chromosome 2.5 The
idea of a fusion is certainly a reasonable proposal within the evolutionary model.
Secondly, the proposed fusion site did not look like those documented in other
mammals.6 Fusions known to occur in animals are characterized by sequences known
as satellite DNA, and most often occur around centromeres. The proposed fusion on
human chromosome 2 was supposedly a telomere-to-telomere fusion, lacking satellite
DNA.
Further, the proposed fusion site did not look like evolutionists expected. It
should have contained long stretches of a tandemly repeated sequence (TTAGGG), but
this pattern was not seen. Instead this sequence was not as prevalent as expected,
and often it was not repeated in tandem (i.e. two or more in a row). This
surprised evolutionists, prompting the question “why are the arrays at the fusion
site so degenerate?”7
There was an additional surprise. The proposed fusion site was surrounded by
unexpected features. For over 600,000 bases surrounding it, there exist many
different types of human-specific genes – none of these genes are found in the
chimp. Telomeres do not contain genes.
In addition to the fusion site, there is supposedly the “remains” of a second
centromere. These were identified based on a type of alphoid sequence that is
commonly found throughout the human genome in many locations, so this sequence is
not specific to centromeres. Thus, it was not too surprising they were able to
find this sequence close to where the “fossil centromere” was supposed to be.4
All this shows that lay-level evolutionary arguments do not necessarily represent
what is known from the scientific literature. In fact, in my experience, the more
compelling the evolutionary story, the less it resembles reality. Evidence doesn’t
speak for itself; it must be interpreted. If someone presents evidence that
appears to contradict the biblical history, one excellent response is to
investigate more fully to see what is going on. In fact, that is what has been
done.
Investigating Further
Further research by creation scientists reveals even more compelling evidence
against the idea that human chromosome 2 was formed by a fusion, much less a fusion
of ape chromosomes. A closer look at the supposed “fossil centromere” has shown
that it is not in the correct location assuming it originated from such a fusion.8
Further, the alphoid sequence in humans (including at the alleged fossil
centromere) does not match the alphoid sequence found in the chimpanzee.8
Focusing on the supposed fusion site itself reveals even more intriguing
information. Using the BLASTN tool, the alleged fusion site aligned (due to
nucleotide similarity of 80% or more) with many regions on human chromosomes and
only a few on chimpanzee chromosomes. However, it did not align with the portions
of the chimp genome that were supposedly involved with the fusion.9
Further investigation revealed that the supposed fusion site encodes a special
region (DNA binding site) within a highly expressed gene.8 This makes sense of the
earlier finding that this region aligned with many regions on different human
chromosomes – since DNA binding sites are found in multiple locations around the
human genome. This gene had originally been characterized as a pseudogene,
supposedly a broken gene. Many pseudogenes are now known to be expressed and have
been shown to carry out important regulatory functions. The gene that the alleged
fusion is located inside is highly expressed in many tissues throughout the human
body. It is also highly networked with many other important genes expressed in the
human body involved in blood cell development and cell signaling. The alleged
fusion site is really a functional feature in the human genome that helps regulate
an important gene – it is not the result of a genomic accident, but has a special
designed purpose.
A More Plausible Explanation of the Evidence
Based on this research, it appears that Dr. Miller’s snide suggestion that “that’s
the way the designer made it”3 is actually a very sensible lay-level summary of the
evidence. The sequence does not match what would be expected by evolutionists, but
instead encodes a portion of a highly expressed gene. Obviously, this fits very
nicely within a biblical worldview. Sure, there could easily have been some
changes to the sequence since the time of creation. However, given its role today,
it is functioning as something that was intelligently designed.
I recently visited Dr. Miller’s website,10 looking for an update by him on the
alleged chromosome 2 fusion since I remembered how vigorously he promoted that
concept. Alas, I didn’t find what I was looking for. Has he begun to doubt common
ancestry between humans and apes? It doesn’t look like it given that his website
still promotes plenty of anti-creation and anti-ID material. This shows, as Ken Ham
pointed out in his debate with Bill Nye, that it is not really about the evidence.
Everyone interprets evidence within a framework, or worldview. If someone does not
wish to consider the possibility of creation, there is no evidence that will ever
convince them.
Footnotes
1. Lightner, J. 2007. A Tale of Two Chromosomes, Answers in Depth 2,
answersingenesis.org/genetics/dna-similarities/a-tale-of-two-chromosomes/.
2. www.youtube.com/watch?v=8FGYzZOZxMw; www.youtube.com/watch?v=zi8FfMBYCkk
3. www.youtube.com/watch?v=zi8FfMBYCkk
4. Bergman, J. and J. Tomkins. 2011. The chromosome 2 fusion model of human
evolution – part 1: re-evaluating the evidence. Journal of Creation 25, no. 2:106–
110.
5. Ijdo, J. W., et al. 1991. Origin of human chromosome 2: an ancestral telomere-
telomere fusion. PNAS 88:9051–9055.
6. Tsipouri, V. 2008. Comparative sequence analyses reveal sites of ancestral
chromosomal fusions in the Indian muntjac genome. Genome Biology 9, no. 10:R155.
7. The idea that the arrays are degenerate is an inference based on assuming the
region resulted from a fusion of primate chromosomes; thus the authors carried in
the belief that the arrays were once there, consistent with interpreting the data
within an evolutionary framework. Fan, Y. et al. 2002. Genomic structure and
evolution of the ancestral fusion site in 2q13-2q14.1 and paralogous regions on
other human chromosomes. Genome Research 12, no. 11:1651–1662.
8. Tomkins, J. P. 2013. Alleged Human Chromosome 2 “Fusion Site” encodes an active
DNA binding domain inside a complex and highly expressed gene – negating fusion.
Answers Research Journal 6:367–375.
9. Tomkins, J and J. Bergman. 2011. The chromosome 2 fusion model of human
evolution – part 2: re-analysis of the genomic data. Journal of Creation 25, no.
2:111–117.
10. www.millerandlevine.com/km/evol
Mouse Memory Enhanced By Humanized “Language Gene”
News to Know
by Dr. Elizabeth Mitchell on September 25, 2014
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Abstract
With mice and men, practice makes perfect, but a mouse with a man’s FOXp2 gene
achieves perfection faster.
News Source
* ScienceDaily: “Neuroscientists Identify Key Role of Language Gene”
We adults envy the ease with which children can learn new languages. How do they
remember what all those words mean and even how to pronounce them? How babies learn
to speak is equally amazing and is still not fully understood. Genetically
engineered mice now offer a clue to these mysteries. Evolutionists also believe
they may explain how humans evolved the gift of gab.
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“The Language Gene”
The gene FOXP2 is so clearly related to speech and language that it has been dubbed
“the language gene.” FOXP2 is a regulatory gene found in humans and many animals—
including primates, mice, birds, and fish. About 700 amino acids long, the protein
FOXP2 encodes in humans differs by only two amino acids from that of chimps and by
only three from mice. Some animals with defective FOXP2 gene are rendered unable to
vocalize properly.
Only humans, of course, have the ability to use language, and FOXP2 is necessary
for normal human speech. FOXP2 regulates many other genes, so how do we know this?
Several members of a Netherlands family with severe difficulty forming words
properly as well as problems putting words together and understanding speech were
found in 2001 to have a defective FOXP2 gene. Now mice with a humanized FOXP2 gene
have revealed a likely role for FOXP2 in learning to produce and understand the
spoken word.
Navigating the Maze
Faced with a T-shaped maze in which only one path leads to a treat, mice are taught
to associate visual clues and the texture of the floor with the correct path. Then
another set of both normal and humanized mice were placed in the maze without the
visual clues. Mice with the humanized FOXP2 (mutant mice), although faster in the
first experiment, did not learn how to choose the right path any faster than
ordinary mice without the visual clues.1 Mutant mice also performed better when
they had to transition from what is called place-based (declarative) to response-
based (procedural) learning; otherwise they performed about the same as the normal
mice. These findings suggest that when there is a scenario where both types of
learning are needed, the humanized version of FOXP2 works better.
Linking Symbols to Reality
The researchers say the following:
Our findings prompt the intriguing speculation that the humanization of this gene
imparted a facilitated ability to use procedural forms of learning and therefore to
shift more rapidly from declarative to procedural forms of learning, a change that
could have been important for the emergence of proficient language and speech.2
The T-maze enables researchers to distinguish between ordinary conditioning and
decision-making through habitual responses to visual clues. FOXP2 may well help
people, infants in particular, learn to habitually use their lips and tongues to
shape words properly. After all, once we learn to speak, we do not usually have to
concentrate on how to pronounce common words!
Furthermore, children are known to form synaptic connections more efficiently than
adults. Since FOXP2 enhances the efficiency of synaptic formation in mice, this
study may even offer us a glimpse into the comparative ease with which children
acquire second languages.
Neurons, Neurotransmitters, and Learning
Earlier research showed mice with humanized FOXP2 genes grew longer dendrites on
some of their nerve cells, made connections between nerve cells better, and had
enhanced dopamine levels in a part of the brain associated with making procedural
memories into habits. But only with this new research have scientists been able to
see what effect these cellular and molecular changes had on actual learning and
performance.
Because FOXP2 operates as a regulatory gene in many parts of the brain, coauthor
Faraneh Vargha-Khadem cautions against extrapolating to the complexities of actual
language acquisition at this point, however, saying, “You can’t extrapolate too
much.”1
Evolutionary Extrapolation
Evolutionary scientists show absolutely no hesitancy to extrapolate beyond the
observable.
In one area, evolutionary scientists show absolutely no hesitancy to extrapolate
beyond the observable—not just to that which remains to be tested but all the way
to the cannot-possibly-be-observed realm of human origins. Evolutionists insist
that humanity’s ancestors diverged from an ape-like ancestor shared with
chimpanzees about 6 million years ago. The FOXP2 protein in humans differs from
that in chimps by only two amino acids. Therefore, some evolutionists hail this
discovery as the mechanism by which two key mutations presumably paved the way for
the human ability to speak.
For instance, senior study author Ann Graybiel explains, “This really is an
important brick in the wall saying that the form of the gene that allowed us to
speak may have something to do with a special kind of learning, which takes us from
having to make conscious associations in order to act to a nearly automatic-pilot
way of acting based on the cues around us.”
Neuroscientist Genevieve Konopka of University of Texas Southwestern Medical Center
comments that this work “provides new ways to think about the evolution of Foxp2
function in the brain. It suggests that human Foxp2 facilitates learning that has
been conducive for the emergence of speech and language in humans. The observed
differences in dopamine levels and long-term depression [i.e. the turning off of
some neuronal activity] in a region-specific manner are also striking and begin to
provide mechanistic details of how the molecular evolution of one gene might lead
to alterations in behavior.”
A Master Switch, not an Information-Generator
FOXP2 protein is a genetic switch. It is a transcription factor that binds to DNA
to control the production of other proteins. It is not possible that FOXP2 could by
switching on any ape-like ancestral genes create the genetic information to evolve
into a new, more complex, more nearly human kind of animal. No mechanism in
genetics has ever been found to do such a thing. FOXP2 can only turn on or off the
information that is already there.
Furthermore, since FOXP2 only controls where and when certain other genes are
active, it does not by itself control or enable language ability. FOXP2 makes it
possible for other developments to take place. The human form of FOXP2 is a
necessary but not sufficient component of linguistic ability.
Liberty University neuroscientist Dr. David Dewitt explains in “FOXP2 and the Non-
Evolution of Human Language,” that even referring to FOXP2 as “the language gene”
is a grossly misleading oversimplification:
Because FOXP2 is a transcription factor, it cannot control language by itself.
Obviously, there are many other proteins involved in the process. Indeed, mutations
of FOXP2 primarily result in impairment of orofacial movements preventing those
affected from making proper word sounds. Afflicted individuals also show some
slight grammar deficiencies. Although the gene is clearly linked to language
production, one cannot designate it as the “language gene.” An analogy would be
calling the mutation that causes muscular dystrophy (and an inability to walk) a
“walking gene.”
Vive La Differénce!
Researchers reporting their results in Proceedings of the National Academy of
Sciences write, “Since the time that the human and chimpanzee lineages separated,
approximately 6 Mya, two amino acid substitutions have occurred in FOXP2, a higher
rate of change than expected given its conservation in mammals.”2
Could two such “substitutions” explain the uniquely human ability to produce and
understand speech? Absolutely not! First of all, arbitrarily defining these two
differences between human and chimpanzee FOXP2 genes as substitutions or mutations
reflects the unverifiable evolutionary assumption that human and chimps share an
ancestor! But being different does not demonstrate mutation from a common ancestral
source!
Interestingly, chimps, gorillas, and macaques have identical FOXP2 proteins.
Evolutionists believe they are separated from mice by 130 million years of
evolution. Yet primate FOXP2 differs from mouse FOXP2 by only one amino acid.
Despite this greater similarity no one claims mice and chimps are close cousins.
The similarity between the FOXP2 in various species points to our common Designer.
It does not demonstrate any sort of common ancestry.
Naturally, humans, chimps, and many other animals share a lot of genes. Despite all
the hype about similarities in chimp and human DNA, that is exactly what we expect
from a wise common Designer, for humans and animals must physically function in the
same world. If anything, we should be impressed that God designed this important
switch to fulfill many roles so perfectly in us and in so many animals.
We look forward to learning more about the designs by which God our Creator
equipped humans alone of all the life He created on the Earth to speak with each
other and with Him. Indeed language helps us sort our thoughts and make sense of
the world. The uniquely human ability to understand and produce language is just
one more reminder that we alone are created in the image of God (Genesis 1:26–27),
and we are indeed “fearfully and wonderfully made” (Psalm 139:14).
Differences Between Chimp and Human DNA Recalculated
Evolutionists Miss the Real Genetic Gap Between Humans and Chimps
by Dr. Nathaniel T. Jeanson on September 17, 2015
Also available in Español
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Are humans less evolved than apes? One recent article implies almost as much:
Humankind likes to believe it sits at the top of the evolutionary tree because of
its complexity, but our success may be down to us actually losing some of our DNA.
Geneticists . . . estimate since early humans split from the common ancestor we
shared with our closest living relatives, chimpanzees, we have lost 40.7 million
base pairs.1
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This recent genetic study2 is just one in a long line of in-depth investigations of
the human genetic code. Like a written language, the human DNA code is based on
four chemical “letters”—A, T, G, and C—that can be arranged in various ways to
carry biologically relevant information. The linear sequence of these letters is
about 3 billion chemical letters long, and in 2001, scientists first elucidated
much of the order of letters in this sequence.3 Since then, many other studies have
attempted to catalog how these 3 billion letters differ amongst the different
ethnic populations around the world.4
On average, each ethnic group differs from another by about 2–4 million single DNA
letters—about 0.1% of the total human sequence (the genome). This recent study
attempted to quantify, not the individual single letter differences, but the
“chunks” of differences. By analogy, if we were to compare two books of differing
editions to each other, we could line them up word-by-word and count the number of
spelling differences. Alternatively, we could compare the books at the sentence
level and quantify the number of whole words or entire sentences that have been
added or deleted between the two editions. The recent genetic study paralleled the
latter.
Unfortunately, rather than stick to an analysis of human genetic variation, the
authors sought to put human genetic differences in the context of man’s supposed
evolution from the primates. To this end, they searched the chimpanzee and
orangutan DNA sequences for chunks of DNA that were (1) shared between chimps and
orangutans and also (2) absent from the human DNA sequence. In doing so, the
authors claim to have discovered that humans lost 40.7 million DNA letters in the
process of evolution from the common ancestor of humans and the great apes.
From a biblical perspective, this conclusion is obviously wrong. The clear and
factual history recorded in Genesis 1 makes it clear that God supernaturally
created humans in His image (Genesis 1:26–28). God didn’t create humans in an
animal image by slowly evolving them from a common ancestor with the apes.
What may come as a surprise to many is that the authors’ conclusions are wrong
scientifically as well. Undergirding the author’s conclusion about DNA “loss” is
the assumption that humans and apes originally shared a common genetic sequence.
Actual genetic data demonstrate a much bigger gap between humans and the apes.
In contrast to the popular assertion that humans and chimpanzees are only 1 to 2%
different, when the billions of letters in each species’ genome are lined up
letter-by-letter, the genetic gap between these species becomes much bigger.
Careful re-tallying of the numbers in the original paper describing the initial
elucidation of the chimpanzee DNA sequence suggests that the two species are only
~89% identical.5 An independent reanalysis of a sample of the raw data concurs with
this assessment.6
Practically, if humans and chimpanzees are 89% identical or 11% different, this is
a gigantic genetic gap. Eleven percent of 3 billion is 330 million. Therefore, a
more accurate answer to the human-chimpanzee genetic similarity question is that
330 million DNA letters separate us from our purported evolutionary cousins. These
differences weren’t “lost” during evolution. The vast majority of them have likely
been present since creation!
In summary, a recent secular publication shows that humans and apes are genetically
different—but not for the reasons that the authors surmise. Humans didn’t “lose”
40.7 million base pairs of DNA in their descent from an ape-like ancestor. We know
from Scripture that humans and apes never shared an ancestor with the apes, and
science confirms this fact. It’s not 41 million differences that separate us from
the primates. It’s hundreds of millions of genetic differences—a difference that
evolution can never bridge!
Seventy Percent of Human Genes Traced Back to Acorn Worm?
News to Know
by Dr. Elizabeth Mitchell on January 7, 2016
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Abstract
Evolutionary scientists claim they have traced the origin of the human throat—and
70% of our genes—back to gill slits and DNA in the lowly acorn worm, “our closest
wormy cousin.” Should we swallow it?
News Source
* Science World Report: “Evolution from Worms: 70 Percent of Human Genes Trace
Ancestry to the Acorn Worm”
* Okinawa Institute of Science and Technology: “Our Closest Wormy Cousins”
* ScienceDaily: “Acorn Worm Genome Reveals Gill Origins of Human Pharynx”
* Huffington Post: “Scientists Map Acorn Worm DNA, and Learn a Lot About Humans in
the Process”
In an effort to discover the characteristics we humans supposedly inherited from
organisms found in the Cambrian explosion, scientists have sequenced the genome of
the acorn worm. “It's an ugly beast,” says UC Berkeley professor John Gerhart,
leader of the project. Coauthor Daniel Rokhsar boldly claims, “Acorn worms are
marine invertebrates that, despite their decidedly nonvertebrate form are
nevertheless among our closest invertebrate relatives.”1
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“Acorn worms look very different from chordates, which makes it especially
surprising that they and chordates, like humans, are so similar on the genomic,
developmental and cell biological levels,” Gerhart adds.2 Chordates include humans
and other vertebrates as well as a few invertebrates, but not acorn worms.
Chordates, if only as an embryo, have a bundle of nerves like a spinal cord
supported by a cartilaginous notochord, a body that extends past the anal opening,
and a series of openings in the side of the throat (pharyngeal slits). Reflecting
the evolutionary presumptions that guide his interpretation of genetic comparisons,
Gerhart says, “I'm interested in the origins of chordates, which, of course, came
from non-chordates, and hemichordates like the acorn worm are the closest we have
to this lineage. So it’s important to compare the development and genomes of our
group, the chordates, with the hemichordates if you want to know what
characteristics the common ancestor really had.”3
“The Mouth Forms Second”
Evolutionists think acorn worms, which have not changed significantly since their
preservation in the Cambrian fossil record,4 are a living representation of the
evolutionary link between vertebrates and invertebrates. All vertebrates and some
invertebrates—like acorn worms—are deuterostomes, a word meaning “the mouth is
second.” The mouth in deuterostome embryos develops “second”—after the opening for
the other end of the digestive tract.5 This “deuterostome” pattern of embryonic
development is found not only in acorn worms but also in starfish, sea urchins,
fish, and all other vertebrates, including humans. Evolutionary scientists believe
that this embryologic pattern is the evolutionary footprint of our shared history
with these animals through a common deuterostome ancestor that presumably lived 570
million years ago.6 This genetic study, in the opinion of the authors, confirms
evolutionary relationships between these very different kinds of animals, as well
as humans.
Of course, the scientists could not actually sequence DNA from a common ancestor of
acorn worms and vertebrates—that ancestor being purely hypothetical, existing only
in their worldview-based imaginations. Instead, Gerhart, Rokshar, Simarkov, and
colleagues sequenced the genomes of two of the 90 or so living species of acorn
worms. Oleg Simakov, coauthor of the study in Nature, says, “Our analysis of the
acorn worm genomes provides a glimpse into our Cambrian ancestors’ complexity and
supplies support for the ancient link between the pharyngeal development and the
filter feeding lifestyle that ultimately contributed to our evolution.”7
Genetic Similarities
The authors of the study report that 8,716 genes have similar counterparts
(homologues) present in enough diverse deuterostomes to “imply their presence in
the deuterostome ancestor.”8 In addition to the discovery that vertebrates and
invertebrates like acorn worms share many protein-coding DNA sequences, the authors
found that some sections of DNA thought to regulate genetic expression appear in
all the different types of deuterostomes they sampled.9 The order in which many
genes are arranged is also similar, suggesting that if certain groups of genes work
together in one kind of animal they often work together in many different kinds of
animals.
The scientists found more genetic similarities between invertebrates than between
acorn worms and vertebrates. Yet depending on how the genes are tallied,10 as much
as 70% of the human genome’s approximately 20,000 genes (DNA sequences that code
for proteins) have counterparts in the acorn worm and hence—by evolutionary
reckoning—with the last common ancestor shared with our so-called “closest wormy
cousin.”11
Of course, we expect to find many common genes in different kinds of animals.
Of course, we expect to find many common genes in different kinds of animals. They
live in the same world in bodies utilizing the same basic biochemistry and sharing
many of the same basic needs. And like genes, many different kinds of organisms
need the same or similar regulatory elements in their genomes. This does not
demonstrate common evolutionary ancestry, just a common Designer—the Creator God.
Furthermore, we are accustomed to hearing that we share about 98% of our genome
with chimpanzees—supposedly our closest primate cousin. Such oft-quoted numbers
are, as Frost Smith explains in “A Fresh Look at Human-Chimp DNA Similarity,”
deceptively impressive. And as Dr. Nathaniel Jeanson points out in “Differences
Between Chimp and Human DNA Recalculated,” evolutionists conveniently overlook the
hundreds of millions of genetic differences that evolution can never bridge.
Acorn Worm
Acorn Worm Diagram
This is an acorn worm. It has many gill slits—shown in blue in the diagram—allowing
water to pass through its mouth and out of its body through gill pores. From this
water an acorn worm not only obtains oxygen—as fish do—but also nutritious organic
debris. The gill slits filter this food from the water. Photograph by user
Necrophorus, via Wikimedia Commons. Diagram by user Zebra.element, via Wikipedia.
Gill Slits—Our Greatest Shared Innovation?
Acorn worms range in size from 3 ½ inches to over 8 feet, and though most species
live in shallow brackish water, some live at the bottom of the sea. The acorn worm
pokes its acorn-shaped proboscis around in sand or mud, stirring up debris. It
directs the debris-laden water into its mouth using cilia and collects not only
oxygen but also bacteria, algae, and other nutritious edible organics by filtering
it through its pharyngeal slits, or gill slits. An acorn worm can have hundreds of
gill slits, equipping it for a very efficient form of filter feeding.
“What’s so great about having gill slits is the large volumes of water you can put
through the animal to collect food; they allow high-throughput filtering and
feeding, whereas other animals take one gulp, deal with the food in that one gulp,
expel the water out the mouth and take another gulp,” Rokhsar explains.12 But the
significance of gill slits in this invertebrate goes far beyond these observable
advantages to the acorn worm and to an evolutionarily minded scientist speaks
volumes about the unobservable past history of many other kinds of animals, and
even humans.
Evolutionists believe that gill slits evolved in animals like acorn worms to make
filter feeding efficient and then later evolved into oxygen-capturing gills and
even later into various parts of our throats that have no direct oxygen-gathering
roles at all. As Rokhsar says, “The presence of these slits in acorn worms and
vertebrates tells us that our last common ancestor also had them, and was likely a
filter feeder like acorn worms today. The pharyngeal area of these worms and of all
deuterostomes is their most significant shared innovation.”13
Neither humans nor other mammals have gills at any point in their development.
Neither humans nor other mammals have gills at any point in their development.
Human embryos have several swellings along the neck, little mounds of cells that
differentiate into parts of the jaw, face, ear, middle ear bones, thyroid and
parathyroid glands, and voice box. Based on superficial appearance and evolutionary
thinking, these folds and swellings were once called gill slits, gill pouches, gill
arches, or branchial arches. Many embryology textbooks have abandoned this
deceptive terminology in favor of pharyngeal arches—meaning “arches in the region
of the throat.” But the authors believe genetic similarities confirm a gill slit
origin for them. That’s why Rokhsar refers to the acorn worm’s gill slits as our
“most significant shared innovation.”
Genes for Such a Worm as I
The authors found that a cluster of six genes expressed during formation of the
embryonic acorn worm’s gill slits corresponds to a cluster of six genes expressed
in a similar anatomical region in many other kinds of deuterostome embryos,
including humans. This cluster of genes consists of coding for four transcription
factors—proteins that control the rate at which various genes are transcribed (from
DNA into RNA)—as well as two common regulatory genes. Though this group of genes is
not found in all the deuterostomes they tested, it was only found in deuterostomes,
and they “conclude that the deuterostome ancestor possessed such a cluster.”14 They
write, “We propose that the clustering of the four ordered transcription factors,
and their bystander genes, on the deuterostome stem served a regulatory role in the
evolution of the pharyngeal apparatus.”15 Rokhsar says, “We think this is an
ancient deuterostome-specific cluster of genes that is involved in patterning the
pharynx.”
This gene cluster is one more piece of evidence affirming the reality of the
Creator we share with all living things.
Well, Rokshar is right in saying that this gene cluster is involved in patterning
the pharynx in many different kinds of deuterostomes—that much is observable! This
gene cluster is involved directing the embryologic development of pharyngeal arches
into sundry different anatomical structures in the neck region of diverse sorts of
invertebrates and vertebrates. But these authors are incorrect in their conclusion
that the common presence of this gene cluster confirms that these invertebrates and
vertebrates share a common ancestor. On the contrary, this gene cluster is one more
piece of evidence affirming the reality of the Creator we share with all living
things. This six-gene cluster, of use directing the embryonic development of so
many different structures in different kinds of embryos, is not evidence of a
shared evolutionary heritage but of a shared Creator.
Do we have acorn worm in our ancestral past? Not at all. Since the same basic
biochemistry operates in all living things on this planet, it is not surprising
that many genes and non-coding DNA sequences are similar or even identical. The
existence of homologous genes, like homologous anatomical structures, does not
scream “evolution” but is readily explained by the fact that all things—from
molecules to man—were designed by the same Creator God.
Footnotes
1. Unversity of California – Berkeley, “Acorn Worm Genome Reveals Gill Origins of
Human Pharynx,” ScienceDaily, November 19, 2015,
http://www.sciencedaily.com/releases/2015/11/151119160524.htm.
2. Ibid.
3. Ibid.
4. As discussed in “Ancient Fossil Looks Like Today’s Acorn Worms,” the variety of
acorn worms found preserved in Cambrian rock by catastrophic burial at the time of
the global Flood varied in that they were able to build a tube burrow, an ability
apparently lost among today’s acorn worms.
5. Bilaterally symmetrical animals (such as insects, mollusks, and annelids) in
which the embryonic mouth forms before the opening at the other end are called
protostomes.
6. This estimated date for the divergence of chordates and non-chordates (like the
acorn worms’ ancestors) from their hypothetical last common ancestor—570 million
years—is derived from molecular clock dating. These dates are based on numerous
unverifiable evolutionary assumptions, including calibration points derived from
the evolutionary interpretation and dating of the fossil record.
7. Catherine Griffin, “Evolution from Worms: 70 Percent of Human Genes Trace
Ancestry to the Acorn Worm,” Science World Report, November 19, 2015,
http://www.scienceworldreport.com/articles/33346/20151119/evolution-worms-70-
percent-human-genes-trace-ancestry-acorn-worm.htm.
8. Oleg Simakov et al., “Hemichordate Genomes and Deuterostome Origins,” Nature
(November 18, 2015), doi:10.1038/nature16150.
9. The study reports the discovery of 6,533 non-coding DNA sections at least 50
base pairs long. (These might have regulatory functions, but that remains to be
determined.) While this number may sound high, we should recall that only a tiny
fraction (around 2%) of the human genome consists of protein-coding segments
(genes). Thus most of the 3 billion base pairs in the human genome are not involved
in the blueprints for proteins. (The ENCODE project has shown, incidentally, that
we should not think of these non-coding parts of the genome as “junk”! Read more
about it in “Decoding the Debris.”) These 6,533 non-coding sections represent a
small though significant portion of these. It is likely that, like genes, many
different kinds of organisms need the same or similar regulatory and other
associated elements in their genomes.
10. The human genome, like other genomes, contains many genes that structurally
resemble genes elsewhere within the genome. These may vary in their DNA sequences
by as much as about 10% and have their own functions, but evolutionists—rather than
considering them part of the genome’s design—view them as mere “copies” and assume
they are evidence that gene duplication provided the raw material through which
novel evolutionary functions evolved. In any case, the existence of such
structurally similar DNA sequences accounts in part for the rather large percentage
of genetic similarity quoted in the paper in Nature. The authors acknowledge this
unverifiable evolutionary presupposition, writing, “Owing to gene duplication and
other processes the descendants of these ancestral genes account for ~14,000 genes
in extant deuterostome genomes including human.” (Simakov et al., “Hemichordate
Genomes . . . ”)
11. Letizia Diamante, “Our Closest Wormy Cousins,” Okinawa Institute of Science and
Technology, November 19, 2015, http://www.oist.jp/news-center/press-releases/our-
closest-wormy-cousins.
12. Unversity of California – Berkeley, “Acorn Worm Genome . . . ”
13. Ibid.
14. Note 9, Supplemental Materials for Simakov et al., “Hemichordate Genomes . . .
” doi:10.1038/nature16150.
15. Simakov et al., “Hemichordate Genomes . . . ”
The Untold Story Behind DNA Similarity
by Jeffrey P. Tomkins on April 23, 2017
Featured in Answers Magazine
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When you hear stories about the astonishing similarity between human and chimp DNA,
there’s something they’re not telling you . . .
“The DNA of humans is 98% similar to chimpanzees.” Who hasn’t heard that claim
before? It’s usually stated as a settled fact and quoted to prove indisputably that
we share a common ancestor.
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But what does this kind of statement really entail, and how do we really know how
similar one creature’s DNA is to another? The answers from my field of research—
genetics—might surprise you.
Not So Fast
While DNA sequencing technology has advanced rapidly over the past 30 years, the
task of determining the entire DNA sequence of a creature’s genome (all its
chromosomes in a cell) and then comparing it to other genomes is anything but
settled. We simply are not in the post-genomics era—as some have arrogantly claimed
—where we have completely sequenced large genomes end-to-end and fully understand
how they work.
Before we can talk about how to compare two organism’s genomes, or their chromosome
complements as they are often referred to, we need to cover a little background
information.
Chromosomes are found in the nucleus of both plant and animal cells. The
chromosomes store the instructions for life in a long chain of information in the
DNA molecule, sort of like computer code. This information is specified by the
order of four small molecules called nucleotides (adenine, thymine, guanine, and
cytosine, referred to as A, T, G, and C, respectively).
Scientists first began determining the sequence of DNA in the 1970s, but the
process was very slow and tedious. Only a few hundred nucleotides out of billions
could be sequenced at any given time, and only small regions of DNA from various
organisms could be sequenced. The technology remained relatively primitive until
the Human Genome Project got off the ground in the 1990s, spurred by the dream of
uncovering the cause for many human illnesses. Government funding to map the human
genome provided the impetus to develop new laboratory technology that drastically
ramped up the speed of the overall DNA sequencing process.
Developing a reliable, complete genome sequence is anything but simple. And
interpreting it correctly is even harder.
But developing a reliable, complete genome sequence is anything but simple. And
interpreting it correctly is even harder. Scientists learned that fact early in the
genomics revolution. They started by attempting to sequence viruses and bacteria
because they were small and much less complex than plants and animals. Then they
moved to the seemingly simple plant and animal genomes, such as fruit flies,
roundworms, and a small weedy plant called Arabidopsis. The task of putting all
this information together into long stretches of contiguous sequence proved
daunting, however.
A Big Mixup
The problem is that the sequencing machines can produce only small snippets of DNA,
called reads. Until very recently, the typical length of an individual sequence was
only about 75 to 1200 bases long. Scientists have to produce billions of these
individual reads to include samples from most of the organism’s chromosomes many
times over. The problem lies in how you stitch these pieces back together.
The genome of a typical mammal, including a human or mouse, is about 3 billion
bases in length. Assembling whole chromosomes out of small snippets is very
challenging, especially if scientists don’t already know a lot about the genome
from previous studies.
Imagine buying 10,000 boxes of the same puzzle, pulling a handful of random pieces
from every box, dumping the pieces into a pile, and then combining them into a
complete puzzle. You get the idea.
For humans, roundworms, and fruit flies, scientists had many genetic resources to
act as a guide or framework to reassemble the DNA. In essence, they could put the
puzzle pieces together by looking at the cover of the puzzle box.
However, in the case of the chimpanzee sequence, they lacked good genetic resources
and funding. So they used the human genome as a framework. They also based this
choice on the evolutionary presupposition that humans and chimps evolved from a
common ancestor. This is a belief, not a fact of science. The obvious outcome of
this approach is that the chimp genome they constructed would be very human-like
even if the actual genome is not.
Moreover, newly published research indicates that the chimp genome is not only
misassembled but likely contains significant contamination from human DNA. It is
now well documented in the scientific literature that many DNA sequence databases
contain significant levels of human DNA from lab workers. In fact, over half of the
DNA sequence data sets used to construct the chimp genome appear to be much more
similar to humans than the rest. (This problem is especially pronounced in the
samples used in the initial stages of the project.)
Of course, having human DNA mixed in would make the final product more human-like
as well.
Okay, But Why the Similarity?
So what about the similarity? As you can see from the way genomes are sequenced,
any claims of similarities demand major caveats. When the genome of one creature is
used to construct the genome of another, then we have a serious problem that
philosophers call “begging the question.” In other words, evolutionists have
produced a chimp genome based on humans and then say it looks similar to the human
genome.
While we won’t know what the chimp genome really looks like until more accurate
research is done, I recently did a study of the chimp reads that have lower levels
of human DNA contamination, and in this newer study the chimp DNA is only 85%
similar to human at best, not 98%.
Yet they’re still “85% similar.” What does that mean?
When comparing genomes, it’s useful to use an analogy of comparing two books. If
you pick two mystery novels off a bookshelf and compare the text using a computer
algorithm, the computer will find many similar isolated words and phrases. Both
books must follow the same rules of grammar (as does every genome), and both books
follow literary conventions that produce an exciting mystery novel (if you like
mysteries). But the similarity does not mean that one book evolved from the other.
Of course, this is a foolish supposition. It’s a natural result of two different
books being designed and written for similar purposes. The same is true of genomes,
which God designed to produce many similar designs, such as bones, organs, and so
on, for chimps and humans to eat similar foods and survive in similar environments.
But we’re still different and fulfill unique purposes.
Another good example is the similarity among computer programs that come from the
same programmer. The programmer doesn’t start from scratch each time he develops a
new program. Instead, he uses the same general commands that he used for other
projects. It shows the creator’s efficiency and ingenuity. We see the same pattern
of both similarity and differences in organisms’ genomes.
Biblical creationists say the similarities in DNA arose because the same Creator
adapted the same basic code for separate created kinds. If a gene in different
creatures encodes a similar protein for a similar biochemical pathway, it’s not
because of evolution, but because of a single programmer. This similarity is a
hallmark of all human-engineered systems, so why would we not expect to see it in
God’s creation?
We need to identify the evolutionary presuppositions that drive many scientists to
interpret the facts in a way that is contrary to Scripture.
Any time we hear claims that conflict with God’s Word, we need to stop and
carefully unpack the facts. Then we need to identify the evolutionary
presuppositions that drive many scientists to interpret the facts in a way that is
contrary to Scripture.
The Bible makes clear that God made different kinds of creatures, including chimps
and humans, from the beginning. The emerging field of genomics is revealing that
God gave chimps and humans similar code to accomplish similar purposes. Yet He also
gave them code that makes each of them unique. The similarities don’t have anything
to do with chimps evolving into humans.
Dr. Jeffrey Tomkins earned a PhD in genetics from Clemson University and served on
the genetics and biochemistry faculty there. He is now director of life sciences at
the Institute for Creation Research. Dr. Tomkins is the primary author of The
Design and Complexity of the Cell.
Finding Adam in the Genome: Does BioLogos Have Even More Egg on Its Face?
by Dr. Nathaniel T. Jeanson on August 10, 2017
Featured in A Response to <i>Adam and the Genome</i>
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Our last post promised to document and detail a strong accusation: that BioLogos
has engaged in systematic scientific error on one of their most prominent
“evidences” for evolution, and that they have misrepresented the arguments for and
against their claims for several years. Today’s post delivers on this promise—
covering the first several years of the controversy.
The Conception of an Idea
In March of 2008, a group of evolutionists published a paper1 on which Venema bases
all of his claims about the supposed existence of an egg-laying “pseudogene” in
humans. In other words, if we think of genes as words, Venema claims that humans
have a misspelled version of a DNA word involved in the formation of egg yolks.
Since chickens lay eggs but humans do not, Venema sees this fact as evidence of
human-bird common ancestry.
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However, the goals of the 2008 study were less audacious. The authors already
assumed that evolution was true, and they simply sought to put more flesh on the
skeleton of mammal evolution. Specifically, using genetics as a tool, the authors
wanted to pin down the details of how placental mammals evolved from egg-laying
ancestors.
The authors specifically claimed to have found three vitellogenin remnants in
humans.
In this paper, the authors used the spatial positioning of various genes in
chickens and other species to identify a likely genetic spot in which to look for
vitellogenin remnants. By analogy to language, it’s like trying to spot an
evolutionary relationship between words by examining the paragraphs and sentences—
the grammatical contexts—in which these words normally occur. Using this approach,
the authors specifically claimed to have found three vitellogenin remnants in
humans.
However, rather than publish the actual percent identity between the chicken
vitellogenin sequence and the purported human vitellogenin sequence, the authors
reported their results in graphical form. By putting the linear sequence of chicken
DNA on the x-axis (at a very zoomed-out level—the actual DNA letters are not
visible) and the linear sequence of human DNA on the y-axis, the authors showed
where human and chicken DNA matched. To make matches between chicken genes and
human genes easier to find, they drew vertical and horizontal lines from each DNA
sequence. All genes (chicken and human) were drawn with green lines, except for one
—the vitellogenin gene, which was highlighted in yellow. In fact, chickens have
three versions of the vitellogenin gene—shown as vit1, vit2, and vit3 in Figures 1–
2.
Where human and chicken DNA matched, small black flecks were drawn. I’ve
highlighted the most relevant sections of these comparisons with gray boxes.
Figure 1
Figure 1. Vitellogenin (vit1) display from 2008 paper. Adapted from PLoS Biol.2
________________
Figure 2
Figure 2. Vitellogenin (vit2 and vit3) display from 2008 paper. Adapted from PLoS
Biol.3
If the chicken and human DNA were nearly identical, you wouldn’t see black flecks
in these gray boxes. Instead, you would see a nearly continuous black line,
indicating high levels of identity between the DNA of these two species. In fact,
as should be apparent in these diagrams, the level of identity between the two
species in this region of DNA was very low.
Exactly how low, the authors never said.
Furthermore, if we draw these diagrams to scale (based on length of the DNA
sequence covered), it should be apparent from these displays that the vit1 (shown
as VIT1 in Figure 3) gene was bigger than either vit2 (shown as VIT2) or vit3
(shown as VIT3) (see Figure 3).
Figure 3
Figure 3. Relative sizes of vitellogenin genes. Drawn to scale. Adapted from PLoS
Biol.4
Together, these results suggested that the vit1 gene held the most potential for
supporting the authors’ claims of human-chicken common ancestry.
The Birth of a Challenge
By May of 2010, Venema was promoting these vitellogenin results as evidence of
evolution. He boldly laid down the gauntlet for all those opposed to evolution:
The mere presence of the mutated remains of a gene required for making egg yolk in
the human genome should give even the most ardent anti-evolutionist pause. That
this gene was found using the prediction of shared synteny [spatial positioning of
genes] between humans and chicken only adds to the impact.5
Venema then took his challenge one step further, impugning the character of those
who disagreed.
Time and again, what we see from Christian anti-evolutionary organizations is not
an attempt to wrestle with the data, but rather to obfuscate it.6
However, Venema never published his own analysis of the 2008 paper. He didn’t
attempt to identify the actual percent identity between the chicken vitellogenin
sequence and the purported human vitellogenin sequence. Instead, he simply cited
the paper and took the results at face value.
Flaunting Pictures of the Baby
By February of 2012, it was apparent that Venema saw this evidence as especially
damaging to creationist views. Instead of just citing the 2008 paper, Venema put
the data on full display.7 However, rather than fill in the void left by the 2008
paper and do his own analysis in order to come up with an exact number, Venema
created his own visual display of the 2008 data.
This is where his problems multiplied. Look carefully at Figure 4. I’ve redrawn the
2008 graph, and overlaid it (to scale) with Venema’s display. In Figure 4, the
horizontal width of either the black flecks (from the 2008 paper) or the cluster of
four boxes on the Homo sapiens (human) line (from Venema’s article) represents the
amount of chicken DNA sequence that matches human DNA. As you can see, Venema
grossly exaggerated the data displayed in the 2008 paper. His boxes are far wider
than the black flecks, making the identity between chicken DNA and human DNA appear
much higher than it actually is.
Figure 4
Figure 4. Comparison of early 2012 Venema diagram to 2008 paper. Adapted from PLoS
Biol.,8 and from BioLogos.9
In September of the same year,10 Venema apparently felt strongly enough about the
vitellogenin data that he decided to take specific creationist organizations to
task. He went so far as to create a table of anti-evolutionary organizations,
complete with their response (or lack thereof) to the vitellogenin claims.
Nevertheless, Venema once again failed to supply an actual number for the identity
between human and chicken vitellogenin sequences. Instead, he published an
alignment of a tiny section of the vitellogenin region from multiple species, and
he also republished what appears to be the same exaggerated chart (Figure 5):
Figure 5
Figure 5. Comparison of later 2012 Venema diagram to 2008 paper. PLoS Biol.,11 and
from BioLogos.12
If the February gauntlet weren’t enough, Venema upped the ante once again:
I would invite these [creationist] groups, all of whom . . . suggest that “junk
DNA” is no longer a tenable idea, to “take the test” and offer an explanation for
the features we observe in the human Vitellogenin 1 pseudogene.13
Egg in the Face?
In October of 2015, the YEC geneticist Jeff Tomkins of the Institute for Creation
Research accepted Venema’s invitation. Tomkins began by doing what no one had done
thus far—reanalyze the raw data and publish an actual number for the percent
identity between the two sequences. Across the vit1 gene region in chickens and
humans, Tomkins found only 39% identity.
This number is even lower than it appears. Because the chemical alphabet of DNA
contains only four letters, the chance of random matches is high. Statistically, in
an alignment of two random DNA sequences, about 25% of them will be identical.
Thus, when we score DNA alignments, we’re not really analyzing the results on a
scale of 1 to 100. Rather, we’re analyzing them on a scale of 25 to 100—a scale of
only 75 points.
If we were to convert Tomkins’ results to a 100-point scale, his reported identity
drops. On a 75-point scale (i.e., on the 100-point scale that we just used, but
which is actually not 100 points because “zero” is not 0% but 25%), the reported
39% identity represents 61 points of difference (100 – 39 = 61) and only 14 points
of identity (39 – 25 = 14). If we divide the latter number into 75, we discover
that the identity is only about 20% (14 / 75 = 19%, which can be rounded to 20%).
Let’s use Venema’s language analogy to understand the significance of these
numbers. For example, we could find words that match in only 20% of their letters.
As an illustration, the word zebra is a five-letter word; since only 1 of its 5
letters matches the word quota,14 these two words are 20% identical.
Is zebra a broken, nonfunctional relic of the word quota?
Venema gives great significance to the way in which the purported human vit1
“remnant” was discovered.
We can take this analogy a step further. In the genetic realm, Venema gives great
significance to the way in which the purported human vit1 “remnant” was discovered.
He thinks that the shared spatial positioning of genes around the vitellogenin
region is added evidence in support of the hypothesis that humans possess a broken
vitellogenin gene. By analogy to language, we could easily imagine two sentences in
which our two words were surrounded by similar words—words would occupy a similar
spatial position in the sentence.
For example, let’s use zebra in the following sentence: “The native habitat of the
zebra is Africa.” Now let’s use its evolutionary relative, quota, in a sentence:
“The hunting of native animals by foreigners has reached its quota in Africa.” I’ve
highlighted in bold the shared words which have the same spatial relationship to
the two words in question—the words the and native both appear in these sentences
before zebra or quota, and the word Africa appears in these sentences after zebra
and quota. By Venema’s logic, these sentences strengthen the evolutionary
relationship between zebra and quota.
Obviously, this claim for an evolutionary relationship between zebra and quota is
nonsensical. How much more so in the vitellogenin example that Venema cites.
In our next article, we’ll observe how Venema’s response to Tomkins creates even
more problems for Venema’s position.
14. Technically, since the English language has only 26 letters, random matches
occur about 4% of the time. Thus, a 1-in-5 match represents a 20% identity on a 96-
point scale. If we were to convert this to a 100-point scale, the identity would be
even lower.
Finding Adam in the Genome: A BioLogos cover-up?

by Dr. Nathaniel T. Jeanson on August 17, 2017
Featured in A Response to <i>Adam and the Genome</i>
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Our last post began to deliver on a promise to document and detail a very serious
accusation: that BioLogos has engaged in systematic scientific error on one of
their most prominent “evidences” for evolution, and that they have misrepresented
the arguments for and against their claims for several years. Today’s post finishes
delivering on this promise.
Wiping off the Mess?
At the end of our last post, we discussed the response of Jeff Tomkins, a young-
earth creationist (YEC) with the Institute for Creation Research, to Dennis
Venema’s claims about the supposed remnants of an egg-laying gene (vitellogenin;
sometimes abbreviated vtg or vit or VIT) in human DNA. We observed that Venema’s
claims were as illogical as the claim that the word zebra evolved from the word
quota. (These two words match at 20% of their letters, just like the chicken vit1
gene and human DNA.) From February to April of 2016, Venema took Tomkins’ claims to
task in a five-part series1 on the BioLogos website. In part one, Venema introduced
the topic and reviewed the evolutionary evidence that he had cited in previous
years. In part two, Venema continued his review, emphasizing again the relevance of
shared spatial positions of genes (a subject which we’ve explored in a previous
post in this series). Remarkably, rather than engage the numbers that Tomkins
published (i.e., numbers that called into question whether a biologically relevant
match actually exists between chicken vit1 DNA and human DNA), Venema simply
doubled down on his (exaggerated and inaccurate) pictorial representation of the
human-chicken vitellogenin match (Figure 1). Again, the horizontal width of either
the black flecks (from the Brawand, Wahli, and Kaessmann 2008 paper2) or of the
black boxes between the Chicken and Human lines (from Venema’s article) represents
the amount of sequence matching between chicken and humans:
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Figure 1
Figure 1. Comparison of 2016 Venema diagram to 2008 paper—vit1. Adapted from PLoS
Biol.3 and BioLogos.4
Now compare this diagram to Venema’s depiction in 2012 (Figure 2; again, the
horizontal width of either the black flecks (from the Brawand, Wahli, and Kaessmann
2008 paper5) or of the boxes on the Human line (from Venema’s article) represents
the amount of sequence matching between chicken and human):
Figure 2
Figure 2. Comparison of later 2012 Venema diagram to 2008 paper. Adapted from PLoS
Biol.6 and BioLogos.7
Do you see how Venema’s diagram changed in 2016? Why did he draw it differently in
2012? Why are his 2016 boxes different sizes? And why do his 2016 boxes still not
match the original 2008 diagram?
Unlike previous years, in 2016 Venema also added his own rendition of the supposed
match between the other chicken vitellogenin genes (i.e., vit2, vit3) and human DNA
sequences. We discussed previously that these sequences are each about four times
shorter than the vit1 sequence. Therefore, numerically, a small visual match in
vit2 or vit3 is less consequential than a small match in vit1. Regardless, with
respect to vit2 and vit3, Venema tried to bring the sequence matches between
chicken and human before his audience (Figure 3):
Figure 3
Figure 3. Comparison of 2016 Venema diagram to 2008 paper—vit2, vit3. Adapted from
PLoS Biol.8 and BioLogos.9
Like his 2016 representation of vit1, Venema’s errors on vit2 and vit3 are not as
egregious as they were for vit1 in 2012. Nevertheless, if you look closely at
Figure 3, you’ll see that Venema’s boxes still don’t quite match the black flecks
from the original paper.
In part three, Venema discusses vitellogenin in the context of other mammal
species, but he provides no numbers—just additional diagrams. Venema claims that
the vitellogenin gene is consistently broken in placental mammals (i.e., mammals
that do not lay eggs), but not in mammals like the platypus that still lay eggs. In
light of this evidence, Venema claims that evolution “has now been tested down to
the molecular level—and has passed with flying colors.”10
Consistent with Venema’s failure to carefully represent and/or read the
evolutionary literature on which he bases his vitellogenin claims, Venema then
proceeds to misrepresent what Tomkins published. For example, Venema claims that
Tomkins “focuses only on one fragment of one of the VIT pseudogenes in the human
genome. This fragment is the largest continuous fragment of the human VIT1 sequence
at about 150 nucleotides long. . . . Note well: this is the only sequence that
Tomkins will address in his paper (!): not the other VIT1 sequence remnants
surrounding this fragment.”11
Had Venema carefully read Tomkins’ paper, Venema would not have made this mistake.
Tomkins clearly analyzed more than the 150-letter vitellogenin fragment:
When the human vtg pseudogene fragment [the 150 nucleotide fragment] was aligned
using very liberal gapping parameters (see Materials and Methods) to the chicken
genomic sequence, sequence identity was only 62%. Genomic DNA surrounding this
fragment was sequentially increased three-fold in size (symmetrically) and each
fragment aligned up to 36,450 bases of human genomic DNA. Sequence identity dropped
as the fragment size increased, eventually leveling off to about 39% identity for a
region of 36,450 bases.12
Venema missed the fact that Tomkins analyzed the 150-letter fragment—and tens of
thousands of DNA letters surrounding this fragment. The 150-letter fragment is not
the only sequence that Tomkins analyzed; Tomkins did indeed investigate the
supposed vit1 sequence remnants surrounding this fragment.
After this egregious error in scholarship, Venema’s attacks only get worse.
Did Tomkins Miss the Main Point?
Venema also finds fault with other elements that he thinks are missing from
Tomkins’ papers. Venema says that Tomkins didn’t give
even a mention of the VIT2 or VIT3 regions with their pseudogene fragments, nor the
flanking DNA also found there. Similarly, the finding that these regions are shared
with a wide array of other mammals is not mentioned. Tomkins has neatly bypassed
the bulk of the evidence with this approach by removing the one fragment he
discusses from its context, and ignoring the VIT2 / VIT3 region altogether.
With respect to vit2 and vit3, the analysis of these genes is indeed missing from
Tomkins’ paper. But upon careful reflection, these omissions make sense. If Venema
had carefully read the original 2008 vitellogenin paper, he would have observed
that the amount of matching between humans and chickens in the vit2 and vit3
regions is even less than that for vit1. (Given Venema’s gross misrepresentation of
the data in the 2008 paper, it would be no surprise if Venema missed this fact.)
Not surprisingly, given the extremely low level of identity—20% (see previous post)
—that Tomkins found for vit1, Tomkins didn’t even bother with vit2 or vit3.
With respect to Venema’s claim that Tomkins removed “the one fragment he discusses
[i.e., the 150-letter fragment] from its context,” we’ve already documented above
that this is factually false. Tomkins analyzed more than the 150-letter fragment,
and Tomkins analyzed tens of thousands of DNA letters on either side of this
fragment.
Pseudogenes lack experiment tests for function.
But what about the fact that Tomkins didn’t deal with vitellogenin genes in other
mammals—both functional vitellogenin genes and vitellogenin “pseudogenes”? Several
considerations cast this omission in a different light. First, since the match
between human and chicken was so poor, why should Tomkins bother with other
species? Second, with respect to functional vitellogenin genes in other species,
creationists have long explained shared functional genes as consistent with common
design—not just with common ancestry.13 Tomkins would have had no need to write a
paper on this finding. Third, with respect to the existence of broken genes in
other mammals, we might first ask if such broken genes exist. (This is what Tomkins
has been asking with respect to vitellogenin “pseudogenes” in humans.) Venema again
provides no numbers—just pictures. However, let’s say that bona fide pseudogenes
exist in mammal species. This would simply bring the argument back to where we
started—to the fact that pseudogenes lack experiment tests for function.
Thus, Tomkins “omissions” are simply logical consequences of the discoveries
Tomkins’ made—and of the already published YEC literature, which Venema doesn’t
seem to read.
What about Venema’s claim that Tomkins “neatly bypassed the bulk of the evidence”?
Venema pulls no punches.
The true “main evidence” for the remains of VIT genes in the human genome is as we
have discussed: the overall match of sequences between placental / marsupial
mammals and egg-laying organisms over large spans of DNA, including flanking
regions. This is the evidence that needs to be addressed—and Tomkins does not even
mention it, let alone address it. It is also highly unlikely that his audience –
since Tomkins is writing not for biologists but rather for laypeople who follow
young-earth creationism—will be able to see this problem in Tomkins’ approach.
Moreover, since Tomkins tells them that this fragment is the extent of the VIT1
pseudogene, they would have to read the original paper [the 2008 paper] by Brawand
and colleagues to notice this is incorrect.14
Is the true “main evidence” the “overall match of sequences between
placental/marsupial mammals and egg-laying organisms over large spans of DNA,
including flanking regions” [emphasis mine]?
Let’s let Venema answer the question himself. In 2010, Venema said that “the mere
presence of the mutated remains of a gene required for making egg yolk in the human
genome should give even the most ardent anti-evolutionist pause.”15 By 2016,
Venema’s true “main evidence” didn’t even include “the mere presence of the mutated
remains of a gene required for making egg yolk in the human genome.” Why did Venema
change his story? Could Tomkins’ publication in 2015 have played a role?
Perhaps Venema’s bold 2010 claims were just a temporary position that Venema later
modified, subsequent to Tomkins publication. This hypothesis is testable. In 2012,
Venema felt so strongly about the “the mere presence of the mutated remains of a
gene required for making egg yolk in the human genome” that he posted two articles
about them.16 Take a look at Venema’s diagrams. Are they depictions of “the overall
match of sequences between placental / marsupial mammals and egg-laying organisms
over large spans of DNA, including flanking regions”? Or are they strictly limited
to the “the mutated remains of a gene required for making egg yolk in the human
genome”? Do you see vit2 or vit3 show up at all in Venema’s illustrations? Or does
he focus on vit1 exclusively? In fact, if the 150-letter fragment is so
inconsequential in Venema’s thinking, why does he display a section of it
prominently in one of his 2012 articles? Why is the “vitellogenin test”—Venema’s
gauntlet for creationists—focused explicitly on “the human Vitellogenin 1
pseudogene,” and not on vit2 or vit3, or even vit1 in other mammals?
In short, from 2010 to 2012, it appears that Venema flaunted his vitellogenin
argument using a very specific line of reasoning. The human-chicken vit1 match—
including the 150-letter fragment—was central to Venema’s arguments. Vit2 and vit3
weren’t even present in his diagrams, let alone the vit genes in other mammal
species. Then, when Tomkins exposed Venema’s arguments as scientifically deficient,
Venema moved the goalposts and emphasized something different.
When Tomkins exposed Venema’s arguments as scientifically deficient, Venema moved
the goalposts and emphasized something different.
Venema claims that “it is also highly unlikely that his audience—since Tomkins is
writing not for biologists but rather for laypeople who follow young-earth
creationism—will be able to see this problem in Tomkins’ approach.” In fact, the
exact opposite is true. Tomkins published a technical paper in which he analyzed
tens of thousands of DNA letters and reported a percent identity value. Venema
simply drew erroneous pictures. Which author is erroneously dumbing down the data
for lay audiences? We could summarize Venema’s entire approach to this question by
slightly tweaking one of his own sentences: it is highly unlikely that Venema’s
audience—since Venema is writing not for biologists but rather for laypeople—will
be able to see this problem in Venema’s approach.
It Gets Messier
In part four of Venema’s response to Tomkins, Venema amplifies his
mischaracterization of Tomkins. He takes issue with Tomkins statements about the
level of DNA identity between chickens and humans in the region surrounding the
supposed vit1 pseudogene. But rather than do his own analysis and report the actual
level of percent identity, Venema simply reposts his erroneous picture (see above)
of the 2008 findings.
To be sure, Venema recognizes that Tomkins’ is basing his numbers on original
research. Venema knows that Tomkins went through effort of obtaining the raw DNA
sequences and electronically comparing them himself. Consequently, Venema attacks
the specific methods that Tomkins uses as “highly idiosyncratic.” Venema doesn’t
give any scientific justification for this accusation. Instead, he refers his
readers to previously published criticisms of Tomkins’ methodologies.
However, if you click the links that Venema supplies and then compare them to
Tomkins’ published paper, you’ll find an incongruity. The published criticisms
attack a method that Tomkins doesn’t even use in his analysis of vit1.17 Yet Venema
concludes, “In any case, Tomkins’ claim in this instance is simply wrong, and would
greatly mislead a non-specialist audience.” In fact, since Venema appears to have
carefully read neither the 2008 paper nor Tomkins’ paper, the misleading is all
Venema’s.
Venema also takes exception to the latter half of Tomkins’ paper. In the latter
half, Tomkins supplies evidence in favor of a function for the purported human vit1
gene fragment. Venema: “The major problem with this argument is that it subscribes
to a false dichotomy: that this sequence is either a VIT1 pseudogene fragment or a
functional part of another gene. From an evolutionary perspective, there is no
issue with it being both.”18
Venema seems to have forgotten the challenge that he laid down a couple years
prior: “I would invite these [creationist] groups, all of whom . . . suggest that
‘junk DNA’ is no longer a tenable idea, to ‘take the test’ and offer an explanation
for the features we observe in the human Vitellogenin 1 pseudogene.”19 Tomkins has
taken Venema’s test, just as Venema requested. Why is this element of Venema’s
challenge suddenly no longer important? Venema seems to have moved the goalposts
again.
By part 5, Venema thinks his rebuttal to Tomkins is sufficient, and Venema moves on
from the vitellogenin evidence. He says so explicitly at the end of part 4: “In the
next post in this series, we’ll leave Tomkins behind and delve into the biology of
how a lineage might shift from laying eggs to placental reproduction.”20
The Cracks Remain
Venema’s next published comment on vitellogenin happened in early 2017—the
publication of the book, Adam and the Genome. This brings us back to where we left
off our discussion of Adam and the Genome—at the end of chapter two. In chapter
two, Venema continues to make the same vitellogenin arguments that he has for the
last several years—with one exception. To be sure, Venema still fails to put an
actual number on the percent identity between chicken vit1 and the purported human
vit1 gene sequence. Instead, he still shows pictures of the supposed sequence
match. But this time, Venema’s picture is different. Once again, the width of the
flecks (2008 paper) or black bars (Venema’s diagram) represent the amount of DNA
sequence matching between chicken and human (Figure 4):
Figure 4
Figure 4. Comparison of 2017 Venema diagram to 2008 paper. Adapted from PLoS
Biol.21 and Adam and the Genome.22
Notice that Venema’s bars appear to bear more resemblance to the flecks of sequence
match shown in the original 2008 paper. Why did Venema’s diagram change? Why did it
take five years for Venema to correct his science? Did Venema finally read Tomkins’
paper (instead of misrepresenting it)? If so, why is Tomkins given no mention? Why
does Venema still refuse to publish any numbers on the actual percent difference
between chickens and humans? If the percent identity is as low as Venema seems to
now (finally) be conceding, why is he still insisting that a bona fide vit1
pseudogene exists?
Let’s consider the significance of the change in Venema’s diagrams from a different
angle. Recall that this entire controversy has been a battle of numbers (Tomkins)
versus pictures (Venema)—to the extent that Venema thinks his diagrams rebut
Tomkins’ numbers. Not only is this unscientific, it is fatal to Venema’s position.
Since Venema treats his pictures as data, Venema has essentially conceded that he
doesn’t understand the scientific data / doesn’t know the scientific data. Why else
would his diagrams (i.e., what he considers data) keep changing? From a scientific
perspective, this is one of the strongest criticisms of Venema’s claims—and it
comes from Venema himself.
Venema’s diagram is, essentially, a tacit admission of error that stretches back
over most of the history of this controversy.
How does Venema’s behavior square with BioLogos’ stated commitment to “humility and
gracious dialogue with those who hold other views”23 [emphasis theirs]? Will Venema
humbly and publicly acknowledge his prior (public) errors? Will he graciously
credit Tomkins for Tomkins’ original research? Will he correct his slanderous
statements about Tomkins’ practice and character? Will he dialogue with Tomkins and
learn the methods that Tomkins is actually employing? Will Venema go back and
correct his earlier articles, to bring his statement on vitellogenin into
agreement? Will Venema tell us what the real main evidence for the vitellogenin
pseudogene is, in a manner that is consistent with Venema’s previously published
statements?
Will Venema humbly and publicly acknowledge his prior (public) errors?
In the book, Venema does none of these things. Why? Because he thinks that YE
creationists are liars. Consistent with this view, he closes chapter two with a
selective quote from a professed YEC. This particular individual claims that
evolution is well-supported by the evidence—Venema thinks that this individual is
simply being “honest” about the evidence—and Venema quotes him towards this end.
What Venema doesn’t tell the reader is the rest of the story. Not surprisingly,
given his professed commitment to the YEC views, the YEC individual was pressed to
offer actual evidence for evolution instead of just asserting that much evidence
exists. He offered none.24
With respect to vitellogenin, Venema’s public behavior is a sad reflection on the
character of BioLogos. Unfortunately, given my many interactions with the members
of BioLogos—in public forums; in written exchanges; in private, hours-long meals
and discussions, etc.—Venema’s actions are not out of the ordinary. BioLogos has
done a tremendous job publicly marketing a clean, gracious, humble image to the
evangelical world; yet I’ve seen a very different (and disturbing) side in private
that is consistent with Venema’s public actions. Venema’s public, documented
actions should serve as a strong warning to all whose only experiences with
BioLogos have been under the guise of BioLogos’ skillfully marketed (but
inaccurate) message of a commitment to “humble and gracious dialogue.”
In summary, we have observed that Venema’s treatment in chapter two of the genetic
evidence for evolution followed exactly what we claimed: Venema fits facts to his
preconceived evolutionary conclusions. In fact, he seems to play somewhat fast and
loose with the facts, as suits his purposes—making the “main evidence” for his
claims one thing in one year and then another thing in another year. He also seems
to have no problem misrepresenting his opponents.
We also discovered an answer to the question from a previous post (i.e., Does
Venema carefully read the evolutionary literature?): it appears that Venema does
not. In fact, his responses to Tomkins makes one wonder if Venema carefully reads
his own claims.
Footnotes
1. Dennis Venema, “Vitellogenin and Common Ancestry—Blog Series,” Letters to the
Duchess blog,
http://biologos.org/blogs/dennis-venema-letters-to-the-duchess/series/vitellogenin-
and-common-ancestry.
2. D. Brawand, W. Wahli, and H. Kaessmann, “Loss of Egg Yolk Genes in Mammals and
the Origin of Lactation and Placentation,” PLoS Biol. 6, no. 3 (2008): e63,
doi:10.1371/journal.pbio.0060063.
3. Ibid.
4. Dennis Venema, “Vitellogenin and Common Ancestry: Understanding Synteny,”
BioLogos (blog), February 25, 2016, http://biologos.org/blogs/dennis-venema-
letters-to-the-duchess/vitellogenin-and-common-ancestry-understanding-synteny.
5. Ibid.
6. Brawand, Wahli, and Kaessmann, “Loss of Egg Yolk Genes . . . .”
7. Dennis Venema, “ENCODE and “Junk DNA,” Part 2: Function: What’s in a Word?,”
BioLogos (blog), September 26, 2012, http://biologos.org/blogs/guest/encode-and-
junk-dna-part-2/.
9. Venema, “Vitellogenin and Common Ancestry: Understanding Synteny.”
10. Dennis Venema, “Vitellogenin and Common Ancestry: Reading Tomkins,” Letters to
the Duchess blog, March 11, 2016, http://biologos.org/blogs/dennis-venema-letters-
to-the-duchess/vitellogenin-and-common-ancestry-reading-tomkins.
11. Ibid.
12. Jeffrey P. Tomkins, “Challenging the BioLogos Claim That a Vitellogenin (Egg-
Laying) Pseudogene Exists in the Human Genome,” Answers Research Journal 8 (2015):
https://answersingenesis.org/genetics/dna-similarities/challenging-biologos-claim-
vitellogenin-pseudogene-exists-in-human-genome/.
13. Nathaniel T. Jeanson, “Does ‘Homology’ Prove Evolution?,” Institute for
Creation Research, http://www.icr.org/article/does-homology-prove-evolution.
14. Dennis Venema, “Vitellogenin and Common Ancestry: Reading Tomkins.”
15. Dennis Venema, “Signature in the Pseudogenes, Part 2,” BioLogos, May 17, 2010,
http://biologos.org/blogs/dennis-venema-letters-to-the-duchess/signature-in-the-
pseudogenes-part-2.
16. Ibid. See also Dennis Venema, “Is there ‘Junk’ in Your Genome? Part 4,”
BioLogos, February 17, 2012, http://biologos.org/blogs/dennis-venema-letters-to-
the-duchess/understanding-evolution-is-there-junk-in-your-genome-part-4; Venema,
“Encode and ‘Junk DNA,’ Part 2: Function: What’s in a Word?”
17. Venema betrays another fact in these citations. Since these criticisms are out
of date (for example, see the following: Jeffrey P. Tomkins, “Documented Anomaly in
Recent Versions of the BLASTN Algorithm and a Complete Reanalysis of Chimpanzee and
Human Genome-Wide DNA Similarity Using Nucmer and LASTZ.” Answers Research Journal
8 (2015): https://answersingenesis.org/genetics/dna-similarities/blastn-algorithm-
anomaly/; Jeffrey P. Tomkins, “Analysis of 101 Chimpanzee Trace Read Data Sets:
Assessment of Their Overal Similarity to Human and Possible Contamination with
Human DNA,” Answers Research Journal 9 (2016):
https://answersingenesis.org/genetics/dna-similarities/analysis-101-chimpanzee-
trace-read-data-sets-assessment-their-overall-similarity-human-and-possible/),
Venema reveals that he doesn’t pay much attention to the young-earth creation
technical literature, a fact to which we alluded previously (see the following:
Nathaniel T. Jeanson and Jeffrey P. Tomkins, “Why Does Mainstream Scientific
Literature Ignore Conclusions from Young-Earth Creationists? Part 4,” Answers in
Genesis, May 25, 2017, https://answersingenesis.org/creation-scientists/mainstream-
scientific-literature-ignore-young-earth-conclusions/; Nathaniel T. Jeanson,
“Creationists Are Liars? Finding Adam in the Genome with BioLogos,” Answers in
Genesis, June 8, 2017,
https://answersingenesis.org/creation-scientists/creationists-are-liars-finding-
adam-in-the-genome-with-biologos/). If Venema doesn’t carefully do his homework on
his opponents, why should we trust his statements about young-earth creation
science?
18. Dennis Venema, “Vitellogenin and Common Ancestry: Tomkins’ False Dichotomy,”
Letters to the Duchess blog, March 24, 2016, http://biologos.org/blogs/dennis-
venema-letters-to-the-duchess/vitellogenin-and-common-ancestry-tomkins-false-
dichotomy.
19. Dennis Venema, “Encode and Junk DNA, Part 2: Function: What’s in a Word?”
20. Dennis Venema, “Vitellogenin and Common Ancestry: Tomkins’ False Dichotomy.”
22. Dennis R. Venema, and Scot McKnight, Adam and the Genome: Reading Scripture
after Genetic Science, Grand Rapids, MI: Brazos Press, 2017.
23. “What We Believe,” BioLogos, http://biologos.org/about-us/our-mission/.
24. Todd Wood, “The Evidence for Evolution,” Todd’s Blog, December 21, 2009,
http://toddcwood.blogspot.com/2009/12/evidence-for-evolution.html.
DNA—The Language of Life
on July 1, 2008; last featured November 21, 2010
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Whenever we hear a foreign language, we may not know what’s being said, but we know
it means something. It isn’t gibberish. The words convey thoughts and meaning by an
intelligent source.
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In recent times, scientists have discovered an unmistakable language within all
living things. Like a miniature library, DNA stores piles of information in
extraordinary molecules that specify the details of everything from the shape of
flower petals to the color of your eyes.
DNA resembles a language in many uncanny ways, as though a supremely intelligent
Author and Life-Giver left His indelible message in every living thing.
The Letters of a Language
Using different combinations of four basic units, called nucleotides, DNA molecules
can store all sorts of information, just like the dots and dashes of Morse code, or
the binary numbers in computers.
The four nucleotides are combined into codes for twenty chemicals known as amino
acids. By rearranging these twenty “letters of the genetic alphabet,” God designed
the language so that it could produce all the proteins that living things need—
humans alone have over 100,000 proteins.
Similarly, English speakers can combine the letters of the alphabet into any words
they need—now numbering hundreds of thousands.
The Letters of a Language
Illustration courtesy of Jon Seest

Unwrapping a Strand of DNA
When it comes to storing massive amounts of information, nothing comes close to the
efficiency of DNA. A single strand of DNA is thousands of times thinner than a
strand of human hair. One pinhead of DNA could hold enough information to fill a
stack of books stretching from the earth to the moon 500 times.
Although DNA is wound into tight coils, your cells can quickly access, copy, and
translate the information stored in DNA. DNA even has a built-in proofreader and
spell-checker that ensure precise copying. Only about one mistake slips through for
every 10 billion nucleotides that are copied. If only our word processors were that
good!
Same But Different
Fingerprint
Interestingly, any two humans are 99% identical at the genetic level. A mere 1%
makes up the many differences we see among people throughout the entire world.
Even if two beings have a copy of the exact same DNA, they are still unique
individuals. For example, even though identical twin babies have 100% identical
DNA, they have different fingerprints. So the invisible Creator makes it clear that
the source of our individuality is not just coded into DNA. We’re not just a bucket
of molecules, but we are unique persons with souls, given to us by the Author of
life.
Genetic Connections with Chimpanzees
on December 4, 2010
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Evolutionists often emphasize our genetic similarity to chimpanzees, but our
genetic connections don’t end there.
News Source
* ScienceDaily: “Plant Clock Gene Also Works in Human Cells”
The correspondence of human and chimp genes is often used as evidence that we share
a common ancestor. Creationists point out, however, that such similarities also
make sense in light of a common designer.
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The circadian clocks found across so many forms of life are often put together
quite differently, despite how similar their ultimate function is.
New research reminds us that many of our genes resemble not only those found in
primates, but also those identified in many other animals and even plants. Plant
biologists at the University of California–Davis have uncovered another genetic
connection in the DNA of the Arabidopsis plant. The gene helps regulate the plant’s
circadian clock, an internal, biologically driven clock that is found in many
plants, animals, and fungi. For example, in humans, the circadian clock helps
determine our bodies’ natural sleep cycles.
The circadian clocks found across so many forms of life are often put together
quite differently, despite how similar their ultimate function is. Nonetheless, the
researchers identified a single gene in Arabidopsis that seems to work exactly like
an equivalent gene in humans. Even more interesting, the plant and human genes were
shown to function so similarly as to stand in for one another. The scientists had
cultured human cells with a deficient copy of the gene. When it was replaced with
the Arabidopsis gene, the human cells worked correctly. Likewise, working copies of
the human version of the gene successfully corrected Arabidopsis cells with broken
copies of the gene.
Such perfect similarity between a human gene and an equivalent plant gene—to the
point where they can be swapped in and out successfully—might seem like solid
evidence for evolution. But there’s a big problem: whereas evolutionists think
chimpanzees and humans share a (relatively) recent common ancestor, animals and
plants supposedly diverged long ago, and the rest of their respective circadian
clocks work very differently. The team therefore explains the gene similarity as a
case of “convergent evolution.” That term is invoked when similar biological
functions, organs, or genes are found in two organisms whose most recent common
ancestor “shouldn’t” have had the shared feature—and, thus, shared ancestry can’t
explain the commonality.
The big problem with convergent evolution is that as we discover more and more
alleged examples, many of which are highly complex, a puzzle arises: if it takes
millions of years of chance and natural selection for such genetically complicated
features to evolve even just once, how likely is it that they evolved more than
once? For that reason, common design is shown to be a superior explanation: God re-
used certain genetic or other biological features when it was appropriate, without
regard for whether it might occasionally look like common ancestry or not.
Odd Non-Man Out
on January 29, 2011
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When considered alongside humans and chimps, the orangutan is the genomic “odd man
out.” Is that because it hasn’t evolved as quickly?
News Source
* ScienceNOW: “Orangutan Genome Full of Surprises”
Thanks to research led by Washington University in St. Louis geneticist Devin
Locke, the orangutan joins the growing list of creatures whose genomes have been
fully sequenced. Because that list includes humans and chimpanzees, Locke’s team
didn’t miss the chance to place the genetic results in the evolutionary framework.
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The biggest “surprise”? While evolutionists believe orangutans split from the
lineage that would lead to humans and chimps some twelve to sixteen million years
ago, the genetic results indicate that orangutan genes have evolved far more slowly
than chimps’ or humans’. While some researchers have tried to link this
differential rate of change to higher intelligence in chimps (and humans), Locke
points out that orangutans are also quite intelligent.
ScienceNOW also reports (as does ScienceDaily) on a study out of Aarhus University
that shows that parts of the human genome are more similar to the orangutan genome
than to the chimpanzee genome. (Though this would be no surprise to evolutionists
who think we are more closely related to orangutans than to chimps.) “[H]umans and
chimpanzees have evolved separately for millions of years,” the report claims. “In
the process, chimps for mysterious reasons lost some orangutan DNA that humans
retained.”
Without the need for a common ancestor, we have no reason to believe chimp and
orangutan genomes diverged from the same starting point.
If we forgo the need to stuff orangutans’ genetic data into the framework of
evolution, a different picture appears. The debate over whether humans are more
closely related to chimps or orangutans breaks down if humans were created
uniquely, and the apparently contradictory similarities we have to both creatures
can be seen as God’s selective, purposive re-use of certain design features.
Apparent differences in the rate of genetic change also evaporate; without the need
for a common ancestor, we have no reason to believe chimp and orangutan genomes
diverged from the same starting point. Therefore the differences need not be seen
as a tally of evolutionary changes, but instead can be understood as, for the most
part, the unique genetic structure God gave these animals at creation.
DNA We're Missing Makes Us Human
on March 12, 2011
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PhysOrg: “Missing DNA Helps Make Us Human” No one, not even evolutionists, disputes
that humans have crossed a threshold that sets us apart from the rest of the animal
kingdom—even chimpanzees, our “close evolutionary relatives.” But according to new
research, it’s actually the genes we don’t have that sets us apart.
A team from Howard Hughes Medical Institute and Stanford University have been busy
scanning human and animal genomes to find out what makes us different—genetically,
that is. Recently, the team located 510 genetic segments that are found in chimps
and other animals but are missing from humans.
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Interestingly, only one of the 510 missing segments disrupts a gene; 509 of the
discrepancies are in the gene-regulating sequences surrounding the actual protein-
coding genes. The researchers believe the missing sequences can account for much of
what makes humans unique, such as our larger brains. For example, many of the
missing sequences were clustered around the genes that help control neural
development.
The team also experimented on mice to further understand the consequences of the
missing genes; one of the stranger results of the differences is that humans lack
sensory whiskers.
Mutations leading to information loss are not incompatible with young-earth
creation, and it is theoretically possible some of the smaller differences could
have arisen naturally.
Although the scientists are cautious, pointing out that there is still much work to
be done to more fully understand what makes us human, they believe the results are
a start. Of course, the idea that the gene sequences have gone “missing” is an
evolutionary artifact. Instead, it seems more reasonable that the differences are
the result of God’s unique creation of humans in His image (Genesis 1:27); however,
mutations leading to information loss are not incompatible with young-earth
creation, and it is theoretically possible some of the smaller differences could
have arisen naturally.
Also of note is that a press release for the news states that we share 96 percent
of our DNA with chimpanzees, while a news release on a related topic puts the
figure at 98.7 percent; for more on this debate, see Greater than 98% Chimp/human
DNA similarity? Not any more.
Turtles Still Baffle Evolutionists
News to Know
on July 23, 2011
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Turtles in search of their long lost ancestor discover genes trump holes in the
head.
News Source
* Nature: “Turtles emerge from their evolutionary shell”
Evolutionary paleontologists and biologists have always found turtles confusing.
Turtles are reptiles, but a confusing array of anatomical and fossil data has left
them in a clade by themselves. (A clade is a group of organisms thought to be
descended from a common ancestor.) Now geneticists are suggesting a molecular tie-
breaker.
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Members of the diapsid clade are defined by the presence of two large temporal
holes in each side of the skull. Crocodiles, lizards, snakes, and dinosaurs qualify
for membership on this basis. Birds have gained membership even though they have
the wrong kind of skull because evolutionists have decided they descended along the
reptile evolutionary branch.
The shell is not the turtles’ only evolutionary puzzle.
The shell is not the turtles’ only evolutionary puzzle. Lacking temporal skull
holes, turtles don’t seem to fit into the diapsid clade. Turtle fossils are dated
by evolutionary paleontologists to the Triassic period 230 million years ago, and
fossilized turtles look just like today’s turtles. Thus far, there is no fossil
evidence to gain the turtle diapsid membership. To account for this discrepancy,
evolutionists have presumed a common reptile ancestor predated even the diapsids.
[UPDATE: In 2014, scientists found that Eunotosaurus, which seems to be an extinct
variety of turtle, has two of these holes, though one is covered by a bone. In 2015
another variety of extinct turtle, Pappochelys, was found to have a diapsid skull.
These discoveries highlight the biodiversity within the created kinds of turtles.]
But turtles may be the next group to get unambiguously promoted to diapsid after
all and even linked to lizard cousins. Previous genetic studies have suggested
turtles were diapsids though they lacked temporal holes. A new genetic study
reported in Biology Letters offers “unambiguous evidence” based on microRNA,
according to molecular paleobiologist Kevin Peterson.
MicroRNA molecules are not involved in protein production but instead regulate the
expression of many genes. Genes which appear to be common to different organisms
can be regulated by specific microRNA molecules, resulting in major morphological
differences. Evolutionists believe that new microRNA molecules can evolve over
millions of years, and they maintain that “once established in a clade they are
rarely lost.”
The latest work found that “turtles and lizards share four unique miRNA gene
families that are not found in any other organisms' genome.”1 Thus researchers are
now confident that turtles and lizards are closely related and that their common
ancestor lost its temporal holes during millions of years of evolution.
As the Common Designer of all things, God created the various kinds of organisms
during the creation week, each fully functional and mature. Many creationists
believe there were at least two created kinds of turtles, and over the past 6000
years “turtle populations have lost genetic information through natural selection
and mutations, so the turtles preserved by the Flood—and those we find today—are
more diverse than the original created turtles, and may well be missing some
features.”2 Furthermore, as the Common Designer, God could utilize bits of
regulatory genes in more than one kind of creature without having those creatures
share a common ancestor.
Incidentally, while microRNA is being used in this instance to support the notion
of a common ancestor, we’d like to point out the enormous differences in the
microRNA found in chimps and humans. A 2006 study of human and chimpanzee brains
discovered 51 microRNA molecules unique to humans and 25 unique to chimps,3 yet one
more reminder of the differences Christ our Creator (Colossians 1:16) built into
the unique biological designs of humans and chimps.
Easy-Going Ape Joins Genome Club
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Easy-going ape joins the genome club.
News Source
* Associated Press: “Scientists map DNA of bonobo, our peaceful ape kin”
The bonobo, an endangered species native only to the region south of the Congo
River in central Africa, is the last great ape to get its genome sequenced.
Comparison with chimpanzee and human genomes reveals the bonobo genome is “98.7%
identical to corresponding sequences in the human genome.”1
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Kay Prüfer of the Max Planck Institute for Evolutionary Anthropology in Leipzig,
Germany, led the sequencing study. Prüfer’s team found the human genome has just as
much in common with the bonobo as with the chimp. "Humans are a little like a
mosaic of bonobo and chimpanzee genomes," says Prüfer. The bonobo and chimp share
an even higher percentage of DNA, 99.6%. The researchers feel this information
should help us understand more about the last common ancestor of all three. They
write, “That ancestor may in fact have possessed a mosaic of features, including
those now seen in bonobo, chimpanzee and human.”2
Chimps and bonobos likely “speciated” from a common ancestor, and there is nothing
about that process that supports ape-to-human evolution.
Prüfer says humans and chimps diverged from their common ancestor 6 million years
ago, but chimps and bonobos did not diverge until a million years ago after being
geographically isolated by the formation of the Congo River. They eventually formed
separate species, though they do resemble each other. Speciation, as we frequently
point out, is observable in nature, does not require millions of years to occur,
and does not involve evolution into new kinds of animals. Speciation is often
associated with such geographic isolation as would have occurred when various
members of the ape kind arrived in Africa after disembarking from the Ark, In other
words, chimps and bonobos likely “speciated” from a common ancestor, and there is
nothing about that process that supports ape-to-human evolution.
The apes’ behaviors differ greatly from each other, but the researchers note each
species has much in common with humans, genetically and behaviorally. Chimps, for
all their cute movie roles, are well suited for the more aggressive roles in which
some filmmakers cast them. Chimps can be fairly aggressive, even quite violent.
They also are competitive and have a male-dominated hierarchy. Chimps, unlike
bonobos, can use tools and have “bigger, better brains.” Bonobo males, on the other
hand, “do not compete intensely for dominant rank” and are often subordinate to
females.3 They “make love, not war” and may bite but never kill. Bonobo society is
a non-violent and playful world of sharing. Bonobos are even nicknamed “hippie
chimps.”4 Geographically isolated from gorillas and chimps, bonobos may have been
able to survive with their non-violent behavior because they faced little
competition for resources. Chimp and gorilla habitats overlap in the wild, possibly
prompting selection for their more aggressive natures.
While the researchers are confident that the behavioral differences will be
explainable genetically, they have not yet investigated those questions. However,
believing that humans are equally related to each of these apes, some scientists
hope this sort of information will explain how the ugly side of human nature
evolved. Brian Hare, who heads the Hominid Psychology Research Group at Duke
University, comments, “Is the bonobo genome the secret to the biology of peace?
They have done something in their evolution that even humans can’t do. They don’t
have the dark side we do. If we only studied chimps, we’d get a skewed view of
human evolution.”
Commenting on the apparent similarity between bonobos and humans, molecular
geneticist and creationist Dr. Georgia Purdom says, “Just as with the chimp genome,
we see numbers reported of over 98% similarity between the bonobo and human
genomes. This shouldn’t be surprising when you understand how the bonobo genome was
sequenced. The scientists used human and chimp genomes as a template or scaffold to
assemble the bonobo genome because of the supposed common ancestry shared by them.
This type of sequencing is very biased and leads to inflated amounts of
similarity.” For more information about the way evolutionary bias affects the
technology used to sequence and compare genomes, see “How Genomes are Sequenced and
Why it Matters: Implications for Studies in Comparative Genomics of Humans and
Chimpanzees” and “Genome-Wide DNA Alignment Similarity (Identity) for 40,000
Chimpanzee DNA Sequences Queried against the Human Genome is 86–89%.”
God created Adam and Eve on Day Six of Creation Week. He made them the same day He
created land animals, including apes. By God’s eyewitness account, therefore,
humans and apes do not share a common ancestor. Speculation about origins is always
influenced by worldview-based presuppositions. Those who reject the possibility of
a Creator must create untestable scenarios built on speculation about the way
genomes of ape-like ancestors could mutate enough to become human. Read more about
this topic in today’s feature on the “Six secrets of you”!
Finally, the origin of humanity’s “dark side” requires we look no further than
Genesis chapter 3. When Eve responded to Satan’s question, “Yea, hath God said?” by
doubting God’s Word, when Adam and Eve rebelled against the Creator—humans acquired
a sinful nature, a “dark nature” God never intended for us to have. Our problem is
sin, not our evolutionary past. The answer to our sin problem is not found in the
genetics lab but in the Cross of Jesus Christ.
Denisovan Human Genome Sequenced
by Dr. Elizabeth Mitchell on January 5, 2013
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Revolutionary DNA sequencing technique said to be “a powerful new tool to fish for
genes that have recently evolved.”
News Source
* Science: “A Home Run for Ancient DNA”
Before leaving 2012 behind, it is worth noting the discovery that headed the
Science Magazine runner-up list for “Breakthrough of the Year.” Ranking just behind
the hitherto elusive Higgs boson and in the same elite group with Curiosity’s
arrival on Mars, the new technique for sequencing ancient DNA discovered by
Matthias Meyer of Germany’s Max Planck Institute for Evolutionary Anthropology made
the 2012 closing headlines. We discussed that discovery here on November 5,
explaining that Denisovan DNA has left a footprint in the genomes of some modern
humans. (This discovery of course is completely consistent with biblical history.
All humans since the time of the global Flood share a common ancestry from Noah’s
family.)
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bone-bit
This tiny replica of the fossilized bit of bone from a Denisovan girl, along with a
couple of teeth, is currently the only known fossil evidence of the Denisovan
people. A new DNA-sequencing technique has unlocked many of its secrets. But which
of those secrets can be read from the DNA, and which are unsupported inferences?
Image credit: copyright Max Planck Institute for Evolutionary Anthropology,
Leipzig, Germany www.mpg.de.
“Ancient DNA” like that recovered from a Denisovan girl’s finger bone and
Neanderthal fossils tends to be degraded to single-stranded fragments. Matthias
Meyer’s method allows those fragments to be sequenced, allowing a more complete
peek at the genome of their long-dead owner. This breakthrough is exciting, but
let’s take a brief look at the reasons it gets kudos from Science Magazine in order
to be better prepared for both the information and interpretations expected in the
new year as the technique is applied to more DNA samples.
Because the Denisovan finger bone and teeth belonged to a human being, the
researchers were able to “read” some of the genetic code. The DNA fragments can be
matched up to their corresponding places on the modern human genome. The Denisovan
girl probably had brown hair and eyes and a brown-toned skin. But what other claims
propelled this discovery to the top-rank in Science Magazine’s eyes? The editors
write:
It also allowed the team to use DNA to estimate that the girl died between 74,000
and 82,000 years ago—the first time researchers had used genomic information to
date an archaic human. The high quality of the genome gives researchers a powerful
new tool to fish for genes that have recently evolved, providing a “near-complete”
catalog of the handful of genetic changes that separate us from Denisovans, who
were close kin to Neandertals.
Can DNA be used to “date an archaic human” with the same reliability as it can be
used to supply the colors for her portrait? Does the fishing expedition for genes
supply evidence of a human evolutionary pathway from ape-like ancestors through
primitive humans to the intellectual paragons of today? The answer to both of these
questions is “no.”
But the inferences about how long ago Denisovans lived are based on unverifiable,
worldview-based assumptions.
Since the Denisovan’s DNA is human DNA, it is reasonable to “read” its information
using what we know of modern human DNA. Conclusions about eye color and recognition
of Denisovan DNA signatures in the DNA of some modern southeast Asian people are
reasonable in light of observable, experimental, operational science. All the
subjects involved in these interpretations are actual humans. But the inferences
about how long ago Denisovans lived are based on unverifiable, worldview-based
assumptions. Molecular clock dating requires not only assumptions that mutation
rates have remained constant but also calibration dates. Those dates are derived
from the scientifically unverifiable interpretations of radiometric dating methods
dictating the age of the layers in which fossils are found. Thus the “clock claims”
about when Denisovans lived are not acceptable.
Evolutionary anthropologists assume that hundreds of thousands of years elapsed
between the evolutionary advent of various Homo species on the earthly scene. And
they assume that humans must have gradually evolved from ape-like ancestors and
through a series of progressively less primitive human forms. Yet nothing about
Denisovan DNA discoveries supports this view. The Denisovans and Neanderthals were
simply humans who lived in the post-Flood world, and like some other varieties of
humans they have left their fossilized remains in Ice Age sediment. Denisovan and
Neanderthal genes are so human because they are human, and their differences with
modern humans are simply human variations. Their lives and their extinction are not
evidence for either molecules-to-man evolution or proof that humans had to evolve
through primitive evolutionary forms.
Chimp-Human DNA Similarity: What Does It Really Mean?
News to Know
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Does genomic information show scientifically that Adam is not our collective
ancestor?
News Source
* World: “Adam VersusCclaims from Genetics”
Claims that chimpanzee and human DNA are 96 to 99% identical are used by
evolutionists as “proof” that chimps and humans are descended from a common ape-
like ancestor. The Human Genome Project—according to the interpretations of
evolutionists—scientifically disproved the possibility of all humans being
descended from one man and one woman. But what does the science really demonstrate?
Westminster Theological Journal recently published an informative essay by
Westminster Theological Seminary professor Vern Poythress, who has a Th.D. as well
as a Harvard Ph.D. in mathematics, refuting these claims.
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The statistical similarity between chimp and human DNA relates primarily to the
portions of DNA that code for proteins, ignoring the vast amount of DNA that has
been commonly called “junk DNA,” sections that now appear to have regulatory and
other functions. Furthermore, understanding how DNA is compared reveals the chimp-
human similarity is not all it seems. DNA consists of millions of “bases”—four
kinds of molecules that act like the letters in a code. But contrary to the
impression given in television programs, sequencing DNA is not a matter of simply
lining up long strings with millions of bases to see what matches.
sequence1
The letters in this short sequence symbolizing a bit of DNA code stand for the
bases: guanine, cytosine, adenine, and thymine. The sequence of such bases encode
not only the instructions for the manufacture of all the proteins in a living
organisms but the instructions regulating the use of those proteins and much more.
Some sections of DNA strands being compared match like this, often because the same
sorts of protein molecules are needed in living organisms. Because DNA consists of
millions of bases, sequencing technology breaks it into short segments for
comparison and then much match up the pieces to be compared, effectively ignoring
the segments that differ greatly. Image by Westminster Theological Journal through
World
As a result of technological limitations, comparisons between chimp and human DNA
focus on areas that are similar. Thus, as Dr. Poythress explains, chimp and human
DNA only appear “99%” identical if:
1. repeated sequences are ignored
2. only sections that “align naturally” are compared,
3. and the only differences noted are single base-pair substitutions.
Thus, extra sequences of DNA—commonly called “insertions” and “deletions”—are
ignored. When they are included among the differences, the figure becomes “96%.”
Note that even these names—insertions and deletions—imply an assumption of
evolutionary modifications by which the DNA of a common ancestor was gradually
modified over time. But the science cannot look back to the genome of an imagined
evolutionary ancestor. And a great deal of DNA, when chimps and humans are
compared, simply does not correspond at all and is therefore completely absent from
the oft-quoted statistics. Furthermore, despite evolutionary insistence that the
chimp is our closest relative, gorilla and orangutan DNA is more similar to ours
than chimpanzee is.
Furthermore, though not covered in Poythress’s essay, when the DNA sequences are
compared more objectively without pre-selecting sequences and filtering the data,
the chimp and human genomes are only about 70% similar.
Even more important than an awareness of the limitations on the statistical
similarity between chimp and human DNA is the ability to understand how
evolutionists interpret what genetic similarity there actually is. Biblical
creationists understand that this is a consequence of having a common Designer who
wisely designed humans and animals to function on earth. Poythress explains:
The most striking genetic similarities between humans and chimps lie in many of the
protein coding regions within the DNA. That is understandable from the standpoint
of design, because proteins are the backbone of chemical machinery inside a cell.
Cells have to have machinery for metabolism, for cell division, for translating DNA
into proteins, for dealing with toxins, and for responding to the environment. The
machinery has to accomplish many of the same things in cells of many kinds, so it
should not be surprising that there are similarities among proteins not only
between man and chimpanzee but throughout the world of living things.
The notion that genetic similarities prove shared evolutionary ancestry is a
consequence of naturalistic Darwinian assumptions superimposed on the data.
Evolutionists assume chimps and humans share an evolutionary ancestry and interpret
all data according to that assumption.
sequence2
When sequences being compared differ by only a different base here and there, those
variations are called “substitutions.” Image by Westminster Theological Journal
through World.
sequence3
When one stretch of the DNA being compared contains a sequence absent from the
other, the difference is called an indel, meaning “insertion-deletion.” Implicit in
the terminology is the assumption that the DNA of each diverged from a common
ancestral form. Image by Westminster Theological Journal through World.
As Poythress says, “Darwinism says that all kinds of living things came into being
by purely gradualistic processes. In the popular mind, and indeed also among many
scientists, Darwinism also involves the additional assumption that the process of
change over time was unguided and purposeless—in other words, God, if He exists, is
absent.”
Yet nothing about the science can confirm that God did not act to create humans and
animals as Genesis chapter one reports, without evolution. And nothing about the
science can demonstrate the evolutionary claim that the origin of life was blindly
naturalistic and purposeless. Poythress explains, “That claim overreaches the
evidence and the competence of science. It is really a philosophical and religious
claim.” Thus, atheism is a sort of “religion.”
Evolutionists assert that population genetics and molecular clocks cannot possibly
point back to just two original people 6,000 years ago. Poythress points out that
the calculations which this claim is based on assume that the human genome has
always had constant rates of mutation and recombination. Population studies further
depend on assumptions about the average lifespans of people. Yet Scripture
indicates that lifespans changed dramatically after the global Flood. The notion
that humanity could not have originated with two created people is rooted in
unverifiable assumptions imposed upon the science.
Given the effects of sin’s curse on humanity, the dramatic changes in lifespan over
a few thousand years, and the population bottleneck that occurred when the global
Flood reduced the genomic variety in the human population to those genes in the
eight people on the Ark, the uniformitarian assumptions on which evolutionary
anthropologists and geneticists base their conclusions that the human population
could not have been traced back to Adam and Eve are faulty.
Thus the science in no way “proves” human ancestry from an ape-like ancestor or the
impossibility of human ancestry from Adam and Eve. As to the age of the earth,
while Poythress writes nothing in his essay to suggest millions of years, in his
opinion, the small variations (“gaps”) in the genealogical lists in the Old and New
Testaments make it impossible to know how long ago God created man. However, a
comparison of genealogical lists reveals that, while there are a few places where
God chose to include and exclude certain people, only some genealogies contain
information about time. And those lists, from which we (and Archbishop Ussher)
derive calculations about the timeline of history, consist of numerically
interlocked data rendering the inclusion or exclusion of a particular person—as far
as the timeline goes—irrelevant. As Dr. Floyd Nolen Jones explains in Chronology of
the Old Testament:
The Scripture precisely lists the age of each patriarch (i.e. Arphaxad = 35 years
old) when the next patriarch (i.e. Salah) is born. Thus, even if the next patriarch
in the recorded genealogy was a great-grandson rather than a son, this procedure of
giving the age of one patriarch when the next is born fixes the two men’s lives
relative to each other. In so doing, it provides an exact continuous chronology
across this time span.1
The father’s (ancestor’s) name is mathematically interlocked to the chosen
descendant; hence no gap of time or generation is possible.2
Furthermore, Jude 14 corroborates the Old Testament genealogies, informing us that
Enoch was a member of the seventh generation from Adam. Scripture does not
contradict itself. Biblical history therefore does reveal that God created Adam and
Eve about 6,000 years ago. And the scientific evidence of hominid fossils, genomic
analysis, and population studies only appear to “prove” evolution if the data are
interpreted expressly by presuming evolution happened. Such reasoning is circular.
Science does not disprove Scripture.
The Trouble with Sequencing
by Dr. Georgia Purdom on November 22, 2006
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The news has been buzzing lately about two recent papers, one in Nature and one in
Science, that are reporting the sequencing of up to one million bases of the
Neanderthal genome.
The news has been buzzing lately about two recent papers, one in Nature1 and one in
Science,2 that are reporting the sequencing of up to one million bases of the
Neanderthal genome.
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The recent papers focus on the sequencing of nuclear DNA rather than mtDNA, which
will be discussed in another article on this website soon. The nuclear DNA was
obtained from a bone sample of a Neanderthal found in Croatia.1 One of the major
problems facing the sequencing of ancient DNA is contamination, from microbes as
well as from those handling the fossils. Since Neanderthals and modern humans are
so closely related, it becomes difficult to discern what DNA is Neanderthal and
what is from modern humans. The researchers used Neanderthal mtDNA to help
determine which bone had the least amount of contamination from human DNA.1
However, what is being used as Neanderthal mtDNA may actually be modern human
mtDNA! Therefore, it makes it difficult to know if Neanderthal nuclear DNA is truly
being sequenced.
Both papers seem to agree that the differences between Neanderthal and modern human
DNA are very small; probably 99.5–99.8% similar (though this is, of course, based
on a very small fraction of the Neanderthal genome). Where there are differences
they think many of these may be due to base damage in the ancient DNA and
sequencing errors. If this is the case it should be very difficult to accept that
Neanderthals are a separate species from humans.
The papers disagree as to whether Neanderthals and humans interbred. The Nature
paper suggests that interbreeding may have taken place, while the Science paper
says interbreeding did not take place. Same evidence, different interpretation!
The papers also claim that humans and Neanderthals diverged (each becoming separate
species) about 500,000 years ago. Again, this is based on many assumptions about
the past for which there is no evidence. For example, the Science paper says:
We assumed that Neanderthals and modern humans evolved from a single ancestral
population of 10,000 individuals and the Neanderthal population split away from the
human ancestral population instantaneously at a time T in the past, with no
subsequent gene flow. [emphasis added]
How do they know? Were they there? Obviously, the answers to those questions are
“They don’t” and “No.” Fortunately, we do have the eyewitness account of God as
given to us in Genesis. God only made two humans, Adam and Eve, and so Neanderthals
(which were clearly human, as discussed in many of our articles) are descendants of
them.
All About the Differences
on April 21, 2007
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* ScienceNOW: “Chimps Are Champs of Genetic Changes”
A sensational headline ran across the science media this week: “Chimps More Evolved
than Humans.” Could it be that there are philosopher-apes out there after all? In
reality, such exuberant headlines referred to a less shocking-yet still unusual-
finding: the chimp genome, according to evolutionists, has undergone greater
evolution since humans and chimps allegedly went separate ways a supposed 7 million
years ago.
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A University of Michigan team led by population geneticist Jianzhi Zhang “compared
nearly 14,000 protein-coding genes in humans and chimpanzees,” identifying only
“154 human genes that have been positively selected,” compared to 233 in chimps.
Because evolutionists believe chimps and humans share a common ancestor, they also
believe that any gene differences between us and chimps are the result of natural
selection “positively” or “negatively” selecting genes. Whatever genes exist now
are considered the “winners” of natural selection; the differences-chimp genes we
don’t have and vice versa-are considered to have been negatively selected.
According to Zhang, whose team’s research was published in this week's Proceedings
of the National Academy of Sciences, chimpanzees’ larger historical population
accounts for the difference. And as for what the difference is all about?
In the chimp, genes that have outpaced those in humans include ones involved in
protein metabolism, gene transcription, and stress response. . . . In the human,
too, the differences appear to be subtle, with selection working rapidly on genes
concerned with fatty acid metabolism and phosphate transport.
Furthermore, “physician-scientist” Ajit Varki of the University of California, San
Diego points out that “[o]ther mechanisms in gene evolution-such as gene
expression, duplication, conversion, and inactivation-are likely to be equally
important” as Zhang’s discovery.
This research serves a few purposes for creationists. First, it’s a good reminder
of just how different humans and chimpanzees are (despite the inaccurate and
misrepresentative “98%+ genome similarity” often cited by evolutionists). Second,
it underscores how morphological homology-that is, similar appearance and
construction-is not an independent sign of evolution; despite superficial human-
chimp similarities, there are complex differences “under the hood.” While
evolutionists see these differences as having arisen in the time since chimps and
humans diverged, it is just as consistent to view our genomes as unique designs of
the Creator, with numerous inherent differences because we are inherently different
creations.
Sponge Synapses
on June 9, 2007
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LiveScience: “Origins of Human Nervous System Found in Sponges”
According to evolutionist scientists, popular cartoon character SpongeBob
SquarePants may not be as fictional a concept as previously thought! Or so suggests
recent research appearing this week in PLoS ONE. The study reviews the recent
finding that “sponges contain about 25 genes that are very similar to human genes
found in the ‘synapses’ of nerve cells[.]” These synapses play a crucial role in
learning and memory, the LiveScience article on the research reports.
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... “sponges contain about 25 genes that are very similar to human genes found in
the ‘synapses’ of nerve cells[.]”
Based on these similar genes, the study’s authors conclude that “the evolutionary
origins of the nervous system are much older than scientists previously thought.”
Sponges, the researchers point out, don’t have nervous systems. Yet in addition to
having “similar” genes to humans, those “similar” genes produce proteins that “were
found to interact with one another in ways similar to proteins in human synapses.”
[emphasis added] Todd Oakley, an evolutionary biologist at the University of
California–Santa Barbara who participated in the research, explained the pattern of
similarity:
“Not only do they have [human synapse genes], they also have this signature that
they may be functioning in a similar way in the absence of a nervous system, as
they do in the presence of one,” Oakley told LiveScience. [emphasis added]
The function of the sponge genes are not clear, but their human counterparts
combine to form complex protein “machines” important for synaptic communication,
Oakley said.
Noticeably, whereas the article describes the genes as “very similar,” Oakley
states categorically (albeit with some editorial alteration) that the sponges have
the human synapse genes. We suspect this is due to Oakley’s (and evolutionists’ in
general) view that if two genes are similar in two organisms that share a common
ancestor (which, ultimately, are all organisms in the evolutionary worldview), the
two genes are presumed to be the same gene, merely mutated in different directions
over eons of supposed evolutionary history. Accordingly, the article notes:
The researchers speculate that the sponge genes were recycled over evolutionary
time, with small modifications, to create the nervous systems of later animals.
The creationists’ view, by contrast, is to emphasize that similarity can never
prove evolution nor disprove creation. Evolutionists explain similarity through
their worldview as the inevitable result of shared ancestry across all life. We
creationists explain similarity through our worldview as the understandable result
of one Designer creating a system of life that shares the same world. Indeed, the
only statement in the article that uniquely supports either creation or evolution
is the final paragraph:
The creationists’ view is to emphasize that similarity can never prove evolution
nor disprove creation.
Other genes would also have had to evolve or to have been co-opted to create
complex nervous systems, such as our own. Scientists think an estimated 77 to 1,000
genes are important for human synaptic communication, Oakley said.
Thus, while similarities are easily explained by creation and evolution, the
differences are only explained well by the creation model; the evolution model,
despite its supposed emphasis on empirical support, has never shown that mutations
increase information—such as yielding the hundreds of genes required just for our
nervous system—as Darwinian evolution requires. While this is interesting
postulation, note that mechanism for the creation of new genes has neither been
described, nor demonstrated, but is apparently blindly believed to have taken
place.
Not Only How Much, But Also How Fast: Gene Sequences
on August 18, 2007
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ScienceNOW: “The 1% Solution”
The inadequacy of similar “genetic potential” in explaining organisms’ similarity
is perhaps most notable in comparisons of chimps and humans, as highlighted by a
ScienceNOW article this week that reported on work published online in Nature
Genetics. “If humans and chimps are 99% alike genetically, how come we're so
different?” asks author Constance Holden, a question answered by the Bible long
before the question was asked. (Of course, the 99% figure is an oft-stated
inaccuracy—see Greater than 98% Chimp/human DNA similarity? Not any more.)
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The latest research indicates that the physiological differences between chimp and
human is caused “not in the proteins that genes produce but in the timing and level
of gene activity.”
The latest research indicates that the physiological differences between chimp and
human is caused “not in the proteins that genes produce but in the timing and level
of gene activity.” Duke University researchers conducted the first-ever “genome-
scale survey of promoter regions,” comparing gene sequences with “nonfunctional
promoter sequences (DNA that by comparison with the chimp and macaque versions
appears not to have been influenced by selection forces)” to establish which
regions appear to have evolved quickly, a sign that the trait the regions promote
are “favorable in human evolution.” Holden explains:
The researchers found that the promoter regions for about 575 human genes—
especially genes involved in brain function and nutrition—have undergone this
selection and are quite different in humans than in chimps.
Unsurprising but still important is the fact that many of the promoter regions that
are the most different are “involved in neural development.” Duke postdoc Ralph
Haygood also notes that that aspect of the discovery is “not surprising, given the
vast differences in behavior and cognitive ability between chimps and humans.”
For evolutionists, this new research is centered around the idea that the
differences in promoter regions are the result of evolution. For creationists, this
new study reminds us that, despite some similarities, God made us different from
apes not only genetically, developmentally, physiologically, and mentally, but also
spiritually.
Chimp Filing for Person-hood
on September 29, 2007
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His name notwithstanding, the current legal case for the personhood of Mr. Matthew
Hiasl Pan (a chimp) is in jeopardy, reports the Associated Press from Vienna,
Austria.
News Source
* LiveScience: “Court Won’t Declare Chimp a Person”
His name notwithstanding, the current legal case for the personhood of Mr. Matthew
Hiasl Pan is in jeopardy, reports the Associated Press from Vienna, Austria. Known
until this summer as just Hiasl, Mr. Pan is facing an uphill battle, it seems, in
being awarded the rights and protections he allegedly deserves. Pan’s legal counsel
has vowed to take the case to Austria’s Supreme Court after a lower court rejected
Pan’s latest appeal.
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So what’s the catch? “Mr.” Pan is actually a chimpanzee (the genus name of
chimpanzee being Pan) who has belonged, for 25 years, to an animal shelter that
recently filed for bankruptcy. Worried that Hiasl and another chimp might end up
homeless, the Vienna-based Association Against Animal Factories (AAAF) wants Hiasl
legally declared a person and given a guardian to “look out for his interests and
provide him with a home.”
The court’s current rejection of the AAAF case is based on the petitioners’ legal
status to represent Hiasl. A court in the UK ruled in April that a British woman
could not be named Hiasl’s guardian because the chimp was neither mentally impaired
nor in danger—at least one of which is required for Hiasl to be given a guardian.
Claiming legal precedence for representation by “close friends,” the AAAF has
appealed the case to the Austrian Supreme Court, which has not yet set a date for
the trial.
AAAF president Martin Balluch “insists that Pan is ‘a being with interests’” and
says the courts are evading the question of Hiasl’s personhood. The AAAF argues
that personhood will “give [Hiasl] the basic rights he needs to ensure he isn’t
sold to someone outside Austria, where he’s now protected by strict animal cruelty
laws.” The AP article notes that the AAAF is not trying to have Hiasl declared a
human, but simply a person:
“The question is: Are chimps things without interests, or persons with interests?"
Balluch [asked]. “A large section of the public does see chimps as beings with
interests.”
It is not immediately clear how much Darwinian perspectives are motivating this
legal action, if at all. But the AP article does note, “[W]ith the genetic makeup
of chimpanzees and humans so strikingly similar, [the AAAF] contends, [Hiasl’s
current situation] just can’t be.”
We do share a substantial portion of our DNA with chimpanzees (though we share half
of our DNA with bananas!), but there are substantial differences as well. Aside
from legal wrangling to further animal protections, the question is, why not grant
chimps legal status? If evolution is true, we simply have different mutations than
chimps, but at heart, are just as much “animal” as they are. Of course, carrying
this to its logical conclusion, we would have to ask why not extend “personhood” to
every vertebrate, or even every animal! (For that matter—and for the atheists to
answer—since we are [supposedly] simply bundles of atoms, how is it right to give
us personhood and deny it to inanimate objects?) Genesis gives us a clear
justification for there to be a difference between humans, animals, and everything
else that God created: humans, Genesis 1:26 notes, are made in the image of God.
However, this by no means gives humankind license to trample the rest of God’s
creation, animals included (Proverbs 12:10).
Group Think
on October 1, 2007
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It’s one of the few areas where creationists and evolutionists agree: all humans
today can be traced back to the same small group of people.
Yet, there are some notable differences. Those who believe in the historicity of
the book of Genesis know that eight people survived a global catastrophe (the
Flood) inside an Ark approximately 4,350 years ago. Meanwhile, secularists are
increasingly accepting the “Out of Africa” belief, which theorizes that a larger
group spread out from Africa some 50,000 to 70,000 years ago.
Researchers took blood samples from Australian Aborigines and Asians and compared
their DNA, tracing paternal/maternal lineage through Y-chromosome DNA and
mitochondrial DNA respectively. The study determined that the branches diverged
some 50,000 to 70,000 years ago.
Although we would dispute the dates, the genetic findings are consistent with the
account of Noah and his family, and the truth of Acts 17:26 that we’re all “one
blood.”
The Parade of Chimps
on October 1, 2007
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A recent headline claims, “Chimps More Evolved Than Humans.” The chimp genome (by
some evolutionists’ thinking) has seen greater evolution than humans since they
went their separate ways seven million years ago.
For the creationist, though, such a claim only reinforces the contention that
chimps have more differences than previously thought. Humans, on the other hand,
are closely related to their first parents on the Ark—Noah and his wife.
More Different Than We Thought
on October 27, 2007
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Although the news has received relatively little attention, scientists publishing
in the journal Genetics last week have showed that “[m]any more genes separate
humans from chimpanzees than scientists believed.”
News Source
* ScienceNOW: “Evolutionary Sprint Made Us Human”
Evolutionists are fond of citing studies that indicate human/chimp DNA similarity
of 98% or greater, and such citations have worked their way into popular culture,
amounting in the eyes of most people as another piece of evidence in favor of
evolution.
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What seems to be less well known is that such estimates are inaccurate because they
exclude other genomic differences. Elie Dolgin reports for ScienceNOW:
It’s often said that there’s only 1% to 2% difference between the genomes of chimps
and humans, two species that had their most recent common ancestor about 5 million
years ago. But that percentage refers to the nucleotide differences in shared
genes.
A team at Indiana University–Bloomington took a “closer look” at gene duplication
and loss in six mammalian genomes, a project that entailed looking at 120,000 genes
in 10,000 gene families. They discovered that gene turnover is
faster in primates than in dogs or in rodents, and even faster in humans, who
swapped genes 1.6 times faster than monkeys and 2.8 times quicker than nonprimates.
Thanks to this rapid change, 6.4% of the 22,000-odd human genes aren’t present in
chimps, making the gap between the two suddenly seem much wider.
The divergence includes a group of brain genes that “more than doubled in size in
humans.”
For evolutionists, the discovery is interpreted as “providing fuel” for natural
selection; after all, in the evolutionary framework, any difference between two
genomes can only be explained by such forces as natural selection and genetic
drift. If humans and chimps have similar genomes, it’s considered a signpost of our
evolutionary lineage; if we have dissimilar genomes, an evolutionary mechanism is
invoked to understand and interpret the dissimilarity. That’s how presuppositions
work: by recasting and interpreting what we observe such that it fits with what we
already believe. For creationists, this news fits perfectly with our understanding
that chimps and humans are unique creations of God, not siblings with a few trivial
genomic differences.
A Tale of Two Chromosomes
by Dr. Jean Lightner on November 14, 2007
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Abstract
There are many anatomical similarities between humans and apes. Our chromosomes are
similar as well. But do human chromosomes hint of chimp ancestry?
Keywords: chromosomes, centric fusions, information, microRNA, science, Dr. Ken
Miller, evolution, centromere, chromosomal rearrangement, information
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Evolutionists can be excellent storytellers. For example, Dr. Ken Miller, a biology
professor from Brown University who testified against Intelligent Design (ID) at
the Dover trial,1 tells an engaging story that he claims is compelling evidence for
evolution. The problem is that because of his naturalistic assumptions, he himself
is unable to distinguish fact from fiction, science from conjecture.
Background
Humans normally have 46 chromosomes. However, sometimes two chromosomes will fuse
together to form one big chromosome. Centric fusions are where two acrocentric
chromosomes (chromosomes with the centromere very close to one end) fuse to make a
large metacentric chromosome (one with the centromere near the middle). It is
estimated that around 1/1000 people carry this type of chromosomal rearrangement.
While they are sometimes associated with problems such as infertility or serious
chromosomal aberrations in the offspring, often they are asymptomatic.2 This is
because all of the necessary information is there in the proper amount; it is just
packaged differently.
The tale of missing chromosomes
There are many anatomical similarities between humans and apes. Our chromosomes are
similar as well. We can see these similarities in the banding patterns of the
chromosomes. One obvious difference between the human and ape karyotype is that
apes have 48 chromosomes (24 pairs) and humans normally have 46 (23 pairs). Dr.
Miller likes to tell an entertaining “who done it” type story asking where the
missing chromosome pair went. He then points out the scientific evidence for a
fusion event on human chromosome 2. There is evidence that implies a fusion event
may have occurred.3 Human chromosome 2 corresponds to ape chromosomes 12 and 13.
Dr. Miller states, “Our chromosome number 2 was formed by the fusion of two primate
chromosomes.”4 Dr. Miller assumes common ancestry and the number of chromosomes is
consistent with his belief. However, he misses other important evidence that
contradicts his basic claim.
Most importantly, reliable eyewitness testimony is more powerful than
circumstantial evidence in establishing historical details. The Bible, inspired by
the Creator himself, indicates that humans were created in the image of God and
distinct from other animals.5 Humans are clearly distinct from other animals in
cognitive and language ability. Occasionally, the ability of chimps to use tools or
simple sign language is touted as evidence for their close relationship with us. In
reality, chimps are not significantly different in these areas from many other
mammals and birds (except that they can use their hands more like us). Chimps lack
the anatomy for human speech. Ironically, a few birds have been known to use human
language quite well, at least for an animal.6 Simple tool making ability is also
seen in a variety of animals.7 While intelligence in animals is quite fascinating,
it is still significantly different from that of humans and gives no hint of common
ancestry. The similarities are much more easily explained by the fact that these
animals all had a common designer who reused certain excellent design elements much
like engineers do in their creations today.
Observed patterns of chromosomal rearrangement
Dr. Miller's enthusiasm about this chromosomal rearrangement may be tied to the
older notion that such mutations are the basis for speciation.8 This belief was
shown to be overly simplistic decades ago when papers appeared describing
chromosomal variations which were not eliminated by selection. One intriguing
example is a single species of rodent (Holochilus brasiliensis) where 26 different
karyotypes were identified in the 42 individuals tested.9 Chromosomal
rearrangements have been identified within many ruminant species. There are
examples in both goats and sheep where individuals with one or more centric fusions
are phenotypically indistinguishable from other animals.10 One researcher who
studied sheep carrying up to three different centric fusions concluded, “It is now
considered that there is little or no evidence to suggest that centric fusions in a
variety of combinations affect the total productive fitness of domestic sheep.”11
So, the bottom line is that centric fusions themselves do not inevitably result in
a new species. It is conceivable that some apes exist with 46 chromosomes. Yet
these animals will be distinctly apes; they will not be “evolving” to become a
human. If the observed evidence is really from a fusion, it is best explained by
the fusion of two human chromosomes.
A diversion from the real issue
The biggest problem with Dr. Miller’s story is that it distracts the audience from
the real issue. It is not the number of chromosomes that is really a significant
difference between humans and apes, but the information contained on those
chromosomes. According to the evolutionary scenario, our apelike ancestors
underwent major anatomical restructuring to develop upright posture, speech
ability, and an astounding increase in cognitive function all by random, chance
processes. Such profound changes were never observed; they are inferred because
evolution has an atheistic basis and assumes there is no creator.
Despite the superficial similarities between human and ape chromosomes, there are
important differences on the molecular level. There are many protein coding genes
in humans that are distinctly human and are not found in chimps. Perhaps more
significantly are the differences in genes that don't code for proteins. Genes have
been described which code for microRNA (miRNA). The miRNA molecule is not
translated, but acts directly to control gene expression. A single miRNA can
regulate the expression of dozens or even hundreds of genes. A study of miRNAs
expressed in the brain found 51 of 447 new miRNAs were distinctly human and 25 were
only found in the chimp.12 The idea that so many genes were altered so that they
are expressed in the proper concentration according to cell type and can
effectively control the many different genes they regulate is not what we would
expect of chance processes.13 It is more rational to believe that God created
humans distinct from chimps, just as He tells us in the Bible.
Blind to alternatives
While the evidence for a fusion appears consistent with the evolution model, Dr.
Miller implies that it is inconsistent with ID or creation models. He makes the
ludicrous claim that the only way creationists can respond to this evidence is:
“That’s the way the designer made it.”4 This statement reveals Dr. Miller’s
inability to think outside his paradigm. As a creationist who finds chromosomal
rearrangements fascinating, I can honestly say I never thought of that possibility.
One possibility I had considered is that humans and apes (and perhaps other animals
too) were created with the same number of chromosomes with similar banding
patterns.14 Since chromosome numbers vary within created kinds, it is not in the
chromosome number where we should expect the most significant differences to lie,
but in the coded information.
Although Ken Miller’s story does not properly consider current scientific
understanding of chromosomal fusions or significant genomic differences between
apes and humans, he promotes it enthusiastically to support his belief that humans
descended from apes. Furthermore, he is ardently opposed to teaching intelligent
design in the schools, claiming that it is not scientific.15 He appears to be blind
to the fact that the belief that humans descended from apes is a religious
(atheistic) one; such changes have never been observed. Thus, he is not able to
distinguish between science and religious indoctrination.
True science and the Bible believer
Despite the misunderstanding and wild story telling of evolutionists, science is
truly a fascinating and rewarding field for Christians who believe the Bible. The
sciences were founded by people with a strong Christian worldview.16 There are
still many fascinating questions waiting to be answered. For example, why do
chromosomal rearrangements occur? It has been pointed out in the literature that
they are non-random.17 Do they have a purpose? (Evolutionists aren't supposed to
ask this.) Do they play a role in speciation? If so, how? Do they help animals
adapt to new environments? Why are there times when they cause problems (i.e. some
carriers have a high percentage of unbalanced gametes18 which results in
infertility or abnormalities in their offspring)? How can they become fixed in a
population? God's world is out there waiting to be explored. The truth is far more
fascinating than fairy tales.
Footnotes
1. Pam Sheppard, “Dover, Pennsylvania (USA) Intelligent Design trial ends today,”
Answers in Genesis, http://www.answersingenesis.org/docs2005/1104dover.asp.
2. F. Morel et al., Meiotic segregation of translocations during male
gametogenesis, Int. J. Androl. 27 no. 4 (2004):200–212.
3. There are patterns of DNA that generally occur at the end of chromosomes which
appear in the middle of chromosome 2 where the fusion is believe to have occurred
(subtelomeric duplications). While there is no second centromere, there are
patterns of DNA found near centromeres that occur in chromosome 2 where the second
centromere is believed to have previously existed (pericentromeric duplications).
Hillier, L.W., et. al., Generation and annotation of the DNA sequences of human
chromosomes 2 and 4, Nature 434 no. 7034 (2005):724–731.
The possibility of human chromosome 2 being the result of a fusion is not a problem
for creationists. It is only the idea that this chromosome was derived from a
nonhuman ancestor that we would take issue with.
4. Ken Miller on Human Evolution, http://www.youtube.com/watch?v=zi8FfMBYCkk.
5. Genesis 1:26–28; 2:7
6. David Catchpoole, “Petulant parrot proves a point—but atheists can’t (or won’t)
see it,” Creation Ministries International,
http://www.creationontheweb.com/content/view/4592/; Ryan Jaroncyk, “Parrot
prodigy,” Creation Ministries International,
http://www.creationontheweb.com/content/view/4901/.
7. Ryan Jaroncyk, “Jumbo Minds,” Creation Ministries International,
http://www.creationontheweb.com/content/view/4713/; A. A. S. Weir, et al., “Shaping
of Hooks in New Caledonian Crows,” AAAS,
http://www.sciencemag.org/feature/data/crow/.
8. Chromosomal rearrangement may play some role in speciation, but it is not
associated with the type of major anatomical rearrangements that ape to human
evolution demands. They also come at a cost, since some DNA is generally lost
during the rearrangements. Also, some rearrangements are associated with
abnormalities. For example, it is estimated that 5% of Down’s syndrome cases are
the result of an extra 21st chromosome carried on a translocation. Ref. 10.
9. M.W. Nachman and Myers, P., “Exceptional chromosomal mutations in a rodent
population are not strongly underdominant,” PNAS 86 no. 17 (1989): 6666–6670.
10. J.K. Lightner, “Changing chromosome numbers,” Journal of Creation 20 no. 3
(2006):14–15.
11. A.N. Bruere and Ellis, P.M., “Cytogenetics and reproduction of sheep with
multiple centric fusions (Robertsonian translocations),” J. Reprod. Fertil. 57 no.
2 (1979):363–375.
12. E. Berezikov et al., “Diversity of microRNAs in human and chimpanzee brain,”
Nature Genetics 38 no. 12 (2006):1375–1377.
13. P. Borger and Truman, R., “Ultraconserved sequences pose megaproblems for
evolutionary theory,” Journal of Creation 21 no. 2 (2007):8–9.
14. While it may turn out that this is not the case, it is fully consistent with a
straightforward interpretation of the Bible. Nothing in Scripture implies that God
must have created different kinds with different chromosome numbers or even
different banding patterns.
15. “A Victory for Science and Education in Dover,”
http://www.millerandlevine.com/dover/index.html.
16. Roger Patterson, Evolution Exposed, (Petersburg, Kentucky: Answers in Genesis,
2006), chapter 1.
17. R. Bandyopadhyay et al., “Parental Origin and Timing of De Novo Robertsonian
Translocation Formation,” Am. J. Hum. Genet. 71 no. 6 (2002):1456–1462.
18. Gametes normally contain one of each chromosome pair. When there is a loss or
gain of chromosomal material during formation, an unbalanced gamete results. This
can be from a missing chromosome, or from a translocated chromosome occurring along
with one (or both) of its homologues. If a translocation is present without either
homologue, then the gamete will be balanced.
If Human and Chimp DNA Are So Similar, Why Are There So Many Physical and Mental
Differences Between Them?
by Dr. Georgia Purdom on September 5, 2006; last featured January 21, 2008
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When studying the human genome and its similarity to that of the chimp, scientists
have recently concluded that 96% of our genome is similar. However, most people are
unaware that this percent pertains to the regions of our DNA that result in
proteins. It seems logical that if a protein performs a certain function in one
organism, then that same protein should perform the same function in a variety of
organisms. This is evidence for a common designer as much as for a common ancestor.
But most of the DNA sequence performs an unknown function and has been largely
dismissed as “junk DNA.” However, increasing evidence supports the view that “junk”
DNA performs an important role. For example, a recent report unexpectedly found
specific sequence patterns in “junk” DNA which scientists have termed “pyknons.”1
It has been suggested that these pyknons may be important in determining when and
where proteins are made.
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Within this “junk DNA” there may be large differences between man and chimp. The
areas of greatest difference appear to involve regions which are structurally
different (commonly called “rearrangements”) and areas of heterochromatin (tightly
packed DNA).
Here are some other interesting differences between the human and chimp genomes
which are often not reported:
* The amount of chimp DNA is 12% larger than what it is in humans.
* Several hundred million bases (individual components of the DNA) of the chimp
genome are still unanalyzed.
* In many areas of the DNA sequence, major “rearrangements” seem apparent. These
account for perhaps 4–10% dissimilarity between chimps and humans.
* Chimps have 23 chromosomes and humans have only 22 (excluding sex chromosomes
for both species).
Thus, the physical and mental differences between humans and chimps are most likely
due to the differences in purpose and function of the so-called junk DNA. This
understanding should leave us more mindful of the awesome complexity of the Creator
and His creation of DNA.
Dr. Georgia Purdom earned her doctorate from Ohio State University in molecular
genetics and spent six years as a professor of biology at Mt. Vernon Nazarene
University. Dr. Purdom is also a member of the American Society for Microbiology
and American Society for Cell Biology.
A Simple Answer
by Peter Galling on September 19, 2008
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Can a simple “yes or no” answer be adequate for a question about Adam and Eve’s
genetic code and today’s human traits?
gymnastics.
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—J., U.S.
If you want a simple yes or no, then no.
Passing the Message
I [had] the privilege of hearing Mr. Carl Kerby speak at my church (First Baptist
Church Seminole, Oklahoma). He was very informative and opened my eyes to a lot of
very useful information. I am sorry that I didn’t get to thank him for his
testimony and his sincere affection for the topics he shared with us. Please pass
this along to him. I will be looking for future events in our region to attend—and
share with others.
—R.R., U.S.
Have Something to Add?
Let us know what you think.
Now that’s the simple answer, and if that’s all you want, J., you don’t need to
read further. However, in some ways “maybe” is a more appropriate answer. We’ve
provided a complete explanation below because explaining our answer to this
question isn’t as simple—some answers just aren’t! So for the logic behind that
answer (we’ll try to avoid verbal gymnastics, though), please read on.
First, a quick overview: the human genetic code is what programs every cell in our
body to do what it does—and thus what gives us many of the physical traits we
exhibit.
In the reproductive process, a sperm cell and an egg cell each contribute 23
chromosomes (made up of DNA) to create a single zygote with 46 chromosomes; these
compose the new map for the developing embryo to follow. Thus, our chromosomes
originate from our parents, who got their genetic information from their parents,
who got it from their parents, who got it from their parents, and so on. Likewise,
we pass on our genetic information to our children, who will pass it to their
children, etc.
Based on the biblical blueprint that we are all descendants of one man and one
woman—Adam (see Acts 17:26 (NIV)) and Eve (see Genesis 3:20)—it would seem
reasonable, then, to conclude that the genetic information in all humans today
ultimately came from Adam and Eve. After all, the only other source would be if God
had created humans again sometime (i.e., separately from Adam and Eve), humans
whose offspring later intermarried with the offspring of Adam and Eve. But the
Bible clearly teaches that this is not the case, as referenced above.1
Now, this would seem to indicate our answer to your question would be a simple yes—
so why did we answer no?
The problem is that, due to the Fall, our bodies don’t always do a perfect job
replicating our genetic information. Instead, there are times when mistakes—
mutations, that is—creep in accidentally. Mutations can be caused by other factors,
too, such as certain types of radiation. Some of these mutations occur in our
somatic cells (e.g., skin cells), and thus, they are never passed along to any
offspring. But if the mutation occurs in a germ cell (i.e., either a sperm or egg
cell) that then fertilizes or becomes fertilized, the mutation will affect the
offspring instead. This is called a germline mutation.
Mutations that result in new characteristics (traits) that weren’t present in the
parent individual are thus “new” genetic traits. The traits would not have been
present in Adam and Eve, but instead arose through mutations along the way;
however, it’s important to note that they are not new genetic information (which
I’ll explain in a moment).
Various factors influence whether the outcome of these mutations is beneficial,
neutral, or harmful. Most are harmful—for example, the many forms of mental
retardation that have hereditary elements; cystic fibrosis; Tay-Sachs; albinism;2
and many other traits (though we would call most “disorders”).
Some traits would be considered relatively neutral. For example, red hair is often
the result of mutations (see How we got red hair (it wasn’t by evolution)); this
would generally be considered neither beneficial nor harmful, though it does
increase the risk of skin cancer (but much less than albinism). Likewise, while
having six fingers on each hand may make it harder to find a pair of gloves that
fit, it is, relatively speaking, a fairly neutral result of mutation-caused genetic
abnormality.
Some mutations may have beneficial outcomes under certain circumstances (note that
this is not through the addition of new information), though they also have
detrimental aspects as well. For example, sickle-cell trait confers reduced
susceptibility to malaria. However, those with this disorder are more likely to
suffer severe problems and even death under other circumstances, such as great
physical exertion, dehydration, and high altitudes, among other deleterious
effects.
But whether the traits these mutations have caused are beneficial, neutral, or
harmful, none of them would have been present in God’s original perfect creation.3
They are all, instead, a result of the Fall, in which Adam’s sin led to corruption
in our world—and in our genetic mechanisms.
But now we get into the confusing world of semantics. We’ve explained that some
genetic traits originated after the Fall, and thus those traits were not present in
Adam and Eve’s DNA, instead having arisen through mutations. However, lest we
confuse any readers, we’re definitely not saying that any new information has been
added to the human genome, and it’s in saying this that we get into some tricky
semantics. How can there be new genetic traits without new information? We’ll use a
brief analogy to explain.
Let’s say I send a short “chain text message” to a friend of mine. The message is
simply “Jan may have just won ten million dollars worth of Zippy Cola! Pass it on!”
Trying to conserve manual exertion as my friend relays the message to his parents
via computer, he types out, “Jan may have just won ten million dollars worth of
Zippy Cola!” They spread the word, and as it spreads on and on, the sentence begins
to change:
* “Jan may have just won ten million dollars worth of Zippy Cola!”
* “Jan may have won ten million dollars worth of Zippy Cola!”
* “Jan may have won ten million dollars wroth of cola!”
* “Jan may have won ten million dollars wroth of cola dollars wroth of cola!”
* “Jan may have won ten million dollars!”
* “Jan m ayhave won ten million dollars!”
* “Jan won ten million dollars!”
* “Jan won ten miloon dollars!”
* “Jan won ten dollars!”
Each sentence is like a different trait in that the ultimate “meaning” is
different. For example, just as the original sentence conveys a very different idea
than the final variation, so the genes coding for brown hair likewise cause the
body to do something different than genes coding for red hair.
However, notice that no new information has been added in our sentence example; all
the information present in the last variation was in the original, even though they
mean different things. There’s also some meaningless junk accumulated along the
way.
So was the mutation that causes cystic fibrosis in Adam and Eve? No. But the gene
that ultimately became mutated (after the Fall) and now causes cystic fibrosis was
present (in Adam and Eve before the Fall). So, in a way the answer to your question
is both “yes” and “no.” And that’s why we would ideally answer “maybe.”
The key points to remember are that, first, we are in no way more physically human
now than we were at creation; second, the human genome has devolved through
mutations and time, such that there is less genetic information, not more; and
third, while not all of the traits present today were present in the Garden of
Eden, they originated sometime after the Curse allowed corruption to creep into our
genome.
gymnastics.
As I’ve described above, the answer is definitely not a simple one. I can’t help
but wonder why you specifically asked us for a simple yes or no and accused us of
“verbal gymnastics.” It is true that sometimes the technical science or philosophy
we write about requires a more complicated response, and we certainly apologize if
you found any of our articles unclear or poorly worded, but by no means do we
attempt to confuse or deceive readers. Rather, we attempt to “demolish arguments
and every pretension that sets itself up against the knowledge of God, and we take
captive every thought to make it obedient to Christ” (2 Corinthians 10:5).
If you do believe that any of our articles have confusing or deceptive passages,
please let us know, and perhaps we can clarify or point you to a better article. A
great place for anyone interested in biblical creation to start is the New Answers
Book, which covers many of the most frequently asked questions we receive.
One final thought: where we succeed in communicating well in our writings,
presentations, and other products, it is a credit to God and His revelation, and
where we fail it is because of our own shortcomings. Perhaps we have articles that
aren’t clear; certainly we have ideas that may ultimately be shown to be incorrect,
although their basis, the Bible, is infallible. Yet insofar as we preach God’s Word
and point people back to the Bible (and God) as the source of ultimate truth, we
have no apologies.
In Christ,
Peter Galling, AiG–U.S.
Footnotes
1. Of course, one could also hypothesize other wild ideas, such as the
possibility of DNA from Nephilim entering the human race—see Nephilim: Who Were
They? for a good analysis.
2. Albinism is considered harmful because of the greater likelihood of skin
cancer and related photophobia.
3. This goes for animals as well. Flightless beetles, polydactyl cats, blind
cave fish, and poodles wouldn’t have been around in Eden, but instead have arisen
through genetic mutations (sometimes with the help of natural selection) since
then.
Time Keeps on Slipping
on April 1, 2007; last featured September 29, 2008
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Cover of Time magazine
Twice in the past five years, our alleged ancestry with apes has made the cover of
Time magazine. All the magazine could offer each time, though, was a lot of
speculation. Neither edition “actually explains how we (or apes) became human,”
observed creationist biologist Dr. David DeWitt of Liberty University.
Similarities of some physical characteristics do not provide evidence of a common
ancestor, as Time claimed; they only provide evidence that the two life forms are
similar. While the writers at Time report that humans and chimps have 98–99%
identical DNA, this is misleading, for they do not mention that there are many
important differences. For example, the percentage obscures the fact there are
about 125 million DNA base pairs that are different between the two.
These reports appear to be renewed efforts by evolutionists to refute the biblical
teaching that man was created in the image of God.
The Question of Y
on July 1, 2010
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We’ve all heard that humans and chimps share up to 98% of their DNA. But new
studies are accentuating the differences between humans and chimps. Research into
one region of the Y chromosome has shown a difference of more than 30%. The
researchers originally believed that human and chimp Y chromosomes would differ
very little, based on their belief that both inherited their Y chromosomes from a
common ancestor.
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Ape
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They are now looking for mechanisms to explain the apparent “rapid evolution” of
the Y chromosome that allegedly caused the 30% difference. They are not, however,
rethinking their evolutionary presuppositions. Their initial conjecture is that
chimps lost several genes after evolving from their common ancestor with humans.
Creationists admit one thing about a possible relationship between chimps and
humans: they have the same Designer. And that presupposition is not open to change.
http://www.sciencemag.org/news/2010/01/y-chromosome-evolving-rapidly
Trace Your Family History through DNA Testing
Taking a Look at the Genographic Project
by Pam Sheppard on March 11, 2008; last featured October 10, 2010
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According to American Demographics, 113 million Americans have begun to trace their
family roots.
In fact, tracing one’s genealogy is second to gardening when it comes to American’s
best loved hobbies. Thanks to rapid advances in technology, the average person can
now use DNA testing to trace his or her own family history. No longer are
genealogist enthusiasts limited to church records, newspaper clippings, and
government censuses.
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Interest in human DNA has skyrocketed since scientists completed the map of the
full human genome in 2003. According to a February 6, 2006, Newsweek article, tens
of thousands of Americans have swabbed their cheeks and mailed in their DNA to
companies nationwide for testing. The Genographic Project, sponsored by National
Geographic and IBM, is one of many organizations that allows individuals to explore
their own ancestral genetic journey using DNA testing. But this group isn’t your
run-of-the-mill DNA testing services. Over the course of five years, this $40
million project seeks to find new knowledge about the history of human migration by
collecting 100,000 samples from people around the world.
For around $100, you can participate in the project. Your personal DNA analysis
will show you how the mutations in your genes identify you as a member of a
specific haplogroup or clan. You can even choose to anonymously contribute your
genetic results to the Genographic Project’s database. Last July, the staff at a
popular secular magazine, Vanity Fair, published each staff member’s haplogroup in
the masthead of their special Africa issue after participating in the project.
How DNA Testing Works
While 99.9% of our genome is identical, it’s the variations found in the 0.1
percent that distinguish us from each other. Geneticists study the two parts of the
genome that remain relatively unchanged as they are passed down: the mitochondrial
DNA (mtDNA), which is passed from mother to children (but is only passed on through
daughters), and Y-chromosome DNA, which is passed down from father to sons.
Occasionally, mutations (spelling mistakes in the language of DNA) occur in the
mtDNA or the Y-chromosome as the DNA is copied and passed from one generation to
the next. Beginning with an individual, these mutations serve as a marker, or
genealogical road sign, and are passed down to that person’s descendants.
Geneticists use these markers from people all over the world to put together one
very large mtDNA or Y-chromosome DNA family tree. Trace the markers backward, and
you can eventually trace back to the approximate geographic region where that
person and his or her descendants first lived.
Not surprisingly, when it comes to tracing our roots back to our original
ancestors, there is some disagreement between evolutionary scientists and
creationists on the timescale and geography of when and where they lived. Consider
the following quote from Spencer Wells, population geneticist and the director of
the Genographic Project: “You got your DNA from your parents, who got it from
theirs, and so on, for millions of generations to the very beginning of life on
earth. If you go far enough back, your genome connects you with bacteria,
butterflies, and barracuda—the great chain of being linked together through DNA”
(“Out of Africa,” Vanity Fair, June 12, 2007).
Like many modern geneticists, Wells starts with the assumption that we all came out
of Africa after humans branched off from their ape-ancestors approximately 5
million years ago. However, the Bible tells us that we were created in the image of
God about 6,000 years ago and that the human population dispersed from Babel with
many likely settling in Africa.
What’s Your Haplogroup?
According to many population geneticists, everyone belongs to a haplogroup or an
ancestral clan. This branch of a family tree includes genetic markers that all have
inherited from a single ancestor. These markers can be traced back to the group’s
most recent common ancestor. Finding out your haplogroup helps you determine the
geographic location from which your ancestors migrated.
DNA Testing Kit
For instance, according to geneticists with the Genographic Project, today around
20 percent of the lineage from eastern African mtDNA belong to haplogroup M1.
Haplogroup B “likely arose on the high plains of Central Asia between the Caspian
Sea and Lake Baikal.” This group makes up around 17 percent of people from
Southeast Asia and around 20 percent of the entire Chinese gene pool.
I recently decided to have my DNA tested with the Genographic Project. For $99.95,
I received a participant kit that included the following items: a DVD about the
project, a map that showed ancient migratory paths, a consent form, and two cheek
swabs and vials. The procedure for collecting my DNA was simple and painless. I
just scraped the inside of both cheeks for 60 seconds and placed the swabs into
separate vials that contained a unique identification number. This number was also
used to track my test results. The only personal information I was asked to provide
was my gender, which lets the laboratory know to check for mtDNA for women or Y-
chromosome DNA for men.
About two weeks after mailing in the kit, I was able to track the progress of the
DNA testing by entering my kit identification number on the Genographic Project’s
website. About six weeks later, the final results were available on their website
for viewing, downloading, and printing.
After receiving the results from your testing, you can also choose to add your
information to the large database kept by Family Tree DNA, a company that helps
families research their family roots through genetic genealogy. They can help you
overcome dead ends in your genealogical research, find out more about your
ancestor’s homeland, and find out if you are related to another family with the
same surname.
When I received my results, I received a map that showed the supposed direction my
maternal ancestors took as they left their homeland in East Africa and dispersed
among the continents. While the interpretation of this migratory path (including
dates and starting point of Africa) reveals many evolutionary assumptions, I did
find the results and the testing process intriguing.
Genographic Map
Starting with “Mitochondrial Eve” in Africa between 150,000 to 170,000 years ago,
the map showed the path taken by various people groups in my ancestral line as they
continued to branch off (including haplogroups Eve, L11/L0, L2, L3, N, R, pre-HV).
The path then led up to my family branch on the tree, haplogroup H.
Genographic Certificate
According to the Genographic Project’s interpretation of my ancestors, their

migration began “about 15,000 years ago after the ice sheets had begun their
retreat [and] humans moved north again and recolonized Western Europe. By far the
most mitochondrial lineage carried by those expanding groups was haplogroup H.
Because of the population growth that quickly followed this expansion, your
haplogroup now dominates the European female landscape.” The results go on to say
that today this haplogroup comprises 40 to 60 percent of the gene pool of most
European populations.
The research my own family had completed confirmed that my maternal ancestors had
European roots, so this was no surprise to me.
The Bible—It Reveals our True Past
While most geneticists interpret the origin and divergence of human population
based on evolutionary assumptions, it shouldn’t surprise us that nuggets of truth
about our real past are being revealed through DNA studies. Even though most of the
geneticists in this field leave out the true author of the story when interpreting
their results, they can follow the “clues” God has given that confirm His Creation.
When we evaluate scientific findings using the best “clue”—His Word—we know all
people descended from Noah and his wife, his three sons, and their wives, all of
whom came from Adam and Eve. Genesis 11 tells us the rest of the story—we came out
of Babel, not out of Africa.
For more information on using DNA testing to trace your roots, see Trace Your Roots
with DNA by Megan Smolenyak and Ann Turner.
Are Pseudogenes ‘Shared Mistakes’ Between Primate Genomes?
by John Woodmorappe on December 1, 2000
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Originally published in Journal of Creation 14, no 3 (December 2000): 55-71.
Abstract
The claim that pseudogenes and their respective variations are shared between
primates in a nested hierarchy, and can only be explained through common
evolutionary descent, is found wanting.
Summary
‘Given a sufficient lack of comprehension, anything (and that includes a quartet of
Mozart) can be declared to be junk. The junk DNA concept has exercised such a hold
over a large part of the community of molecular biologists …(emphasis in
original).’ – Zuckerkandl and Henning1
‘DNA not known to be coding for proteins or functional RNAs, especially
pseudogenes, are now at times referred to in publications simply as nonfunctional
DNA, as though their nonfunctionality were an established fact.’ – Zuckerkandl,
Latter and Jurka2
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The evolutionary claim that pseudogenes and their respective variations are shared
between primates in a nested hierarchy, and can only be explained through common
evolutionary descent, is found wanting. Evidence for pseudogene function continues
to accumulate, and is much more significant than the actual number of known
functional pseudogenes. In addition, pseudogene-related phenomena show considerable
differences between ‘close’ primates, and are neither self-consistent nor in
agreement with other phylogenetic interpretations. Furthermore, pseudogene
deployment and alteration are governed by strongly non-random events. Unless
evolutionists can rigorously demonstrate that pseudogene-related phenomena cannot
occur independently in different primates, their ‘shared mistakes’ argument should
be rejected.
The human genome is believed to be littered with pseudogenes, which are gene-like
structures that do not code for proteins because of some presumed defect.3 A
recently-published4 abridged example is shown (Table 1). Useful summaries on this
topic are available.5,6 The term pseudogene, as used here, encompasses both the
classical and the retroposited varieties, the latter of which includes interspersed
repeats*, notably SINEs* and LINEs*.7 Creationist scientists (including me)
generally assume that God would not create purposeless genes in different primates,
and that God did not independently disable the same genes in humans and nonhuman
primates during the Curse.
Figure 1
Figure 1.Schematic illustration of orthologs and paralogs. A, B, C and D represent

any combination of mutually-similar and presumably-related genes and/or
pseudogenes. A and B are always paralogs of each other, as are C and D. Depending
upon degree of similarity (and therefore perceived evolutionary relatedness), the
following orthologous pairings are possible: (A, C), (A, D), (B, C) or (B, D). Only
the first and fourth, or second and third, orthologous pairings can simultaneously
coexist.
Unfortunately, the distinction between empirical observation and evolutionary
interpretation is often particularly difficult in molecular biology. There is
always an element of subjectivity in the process of aligning sequences of
homologous (orthologous*) DNA8,9 (Fig. 1), and this is aggravated by non-
corresponding segments of the same.10 Furthermore, it is unclear just how close the
resemblance must be to rule out a fortuitous match-up of mistakenly orthologous
sequences. For instance, there is ambiguity11 about the status of one 34 bp (base-
pair*) segment exhibiting 68% nucleotide* correspondence between the human and rat
genomes. And last, molecular similarities, including those of pseudogenes, do not
create self-evident truths, but must be interpreted:
‘At face value, this is just wrong—alignment procedures delineate similarity
between sequences but tell us nothing about their common ancestors, if such ever
existed. To give an absurd but relevant example, poly-A* tails of any two processed
pseudogenes are perfectly alignable, but it would be a stretch to consider them
homologous.’12
Contrary to the assertions of some,6 the presumed temporal persistence of
supposedly-useless pseudogenes actually constitutes a serious problem for
evolution. The manufacture of DNA is energetically costly to the cell, and natural
selection should remove DNA were it actually useless.13 A mechanism for removal is
now known.14
If they are actually selectively neutral and subject to random mutations, ‘old’
pseudogenes should in fact be scrambled beyond recognition. Apropos to this,
orthologous SINEs have now been found in different phyla,15 and the cited
researchers recognize that the (evolutionary) maintenance of a close correspondence
between such phylogenetically*-distant organisms is very difficult to explain if
SINEs are of no use to their carriers. More on this later.
Table 1
Table 1. Aligned sequences of Cytochrome b and mitochondrial-related pseudogenes.

From Moreira and Seuanez (1999). Base abbreviations are as follows: A-adenine, C-
cytosine, G-guanine and T-thymine. The 301-member sequence is demarcated by tens
(*) and hundreds (**). Nucleotides identical to human are denoted (.).
Click thumbnail to view the entire table.
I. Are pseudogenes useless?
If pseudogenes are functional, they are no different from any other homologous
structure found in nature. These all reflect the fact that God used the same
‘blueprint’ or ‘art form’ repeatedly when constructing different living things. In
this case, the orthologous placement of pseudogenes, and their respective
differences, are moot.
The importance of pseudogene-caused genetic diseases6 is apt to be exaggerated
because, by their very nature, deleterious retroelements* are so obvious.16 The
opposite is the case with beneficial pseudogenes. In fact, for at least some
pseudogenes, failure to observe them coding a product under experimental conditions
is not ipso facto proof of their inability to do so:
‘In these and other examples it cannot be stated with certainty that a gene is
unequivocally either a pseudogene or a gene. It is possible that analysis has not
been performed in the appropriate temporospatial conditions to detect
expression.’17
One argument adduced in support of pseudogene nonfunction is the observation that
they contain many more nucleotide differences (which are assumed to be mutations),
and are more variable in terms of base-pair composition than their paralogous*
protein-coding genes. Yet this observation is compatible with function.2 In fact,
as mentioned below, an ability to code for a product useful to the host organism
hardly exhausts the possibilities for pseudogene function. It is interesting to
note that the inferred nucleotide-substitution rate in pseudogenes shows only crude
correspondence with primate phylogeny, for which reason it has to be manipulated
post hoc by up to tenfold18–20 in order to contrive an agreement between the timing
of different episodes of primate evolution. Pseudogenes whose age is deduced on the
basis of the numbers of nucleotide differences from their coding paralogs show only
a weak relationship between age and the numbers of indels*.21 Each branch of the
phylogenetic tree, of pseudogenes relative to primate evolution, exhibits widely
divergent rates of indel formation.22
It is interesting to note that there are some pseudogenes which cannot be
straightforwardly portrayed as inactivated copies of their paralogous genes. This
includes the human AS pseudogenes, each of which shares a concerted pattern of 19
nucleotides that sets it apart from its inferred gene paralog.23
A large and rapidly-growing body of evidence for pseudogene functionality exists,
most of which will be presented in a forthcoming paper.24 Earlier-known evidences
are given elsewhere.5 There is a theory25 which proposes that pseudogenes interact
with antisense RNA*. The functionality of Alu* units has long been suspected,26 and
recently confirmed.27,28
The distinction between ‘processed genes’ and ‘processed pseudogenes’ is not,
contrary to one critic,6 the result of creationist confusion, but is instead the
product of the critic’s semantics. After all, the former is but a functional
version of the presumably-nonfunctional latter.29 Evolutionists assume that certain
retropseudogenes have become ‘recruited’ by evolutionary processes and are thereby
secondarily functional. These are called processed genes. But this of course begs
the question about them having lost function to begin with! The claim6 that
functioning pseudogenes are manifestations of beneficial mutations is also an
egregious act of begging the question. The latter also reflects the following
prejudicial and erroneous notion: if ‘crippling mutations’6 prevent a protein-
coding function, this is ipso facto synonymous with no function.
A numbers game? Depreciating evidences of pseudogene function
Max’s response6 to this evidence is to use the ‘ATT’ (Appeal to Technicalities)
fallacy and the ‘ATM’ (Appeal to Marginalization) fallacy.30 Each is described in
turn.
Users of the ATT fallacy engage in much post hoc quibbling about the broad
applicability of contrary evidence.31 One example32 is the belittling of the
discovery of ‘junk DNA’ function33 by pointing out the (correct) fact that this
noncoding DNA differs from that in pseudogenes. But discoveries of this nature, and
successive ones,34 cannot be dichotomized so easily (see Abstract). This is
especially so in light of the fact that the identical ‘nonfunctional unless proven
functional’ mentality besets our understanding of all types of noncoding DNA.
Finally, and as noted earlier (and especially in the forthcoming paper24), evidence
for function is not limited to generic ‘junk DNA’, but is now known for
representatives of all the major types of pseudogenes. Therefore, attempts to
depreciate the significance of such function (as by asserting that it is only true
of a few processed pseudogenes6) appears to be another use of the ATT fallacy.
The ATM fallacy treats evidence as a simple numbers game.35 But, as pointed out by
the philosopher of science Sir Karl Popper,36 evidence cannot be treated in this
way (e.g. as so many points for, versus so many points against, a theory). Indeed,
one contrary observation is often sufficient to falsify a theory. Popper’s
philosophy clarifies the fact that, contrary to Max,6 the ‘nonfunctional
pseudogenes’ argument is not substantiated by large numbers of apparently
nonfunctional pseudogenes, but is instead falsified by a significant and rapidly
growing body of evidence which demonstrates such function.
II. The overall nonfunction of pseudogenes: established or tentative?
In response to those who assume that pseudogene nonfunction is well established,6
we must consider several factors, not the least of which is the following:
‘Science is supposed to advance step by step, with all conclusions supported by
adequate evidence. Yet conclusions are sometimes widely accepted without much
evidence, and woe to those who come along later with data supporting what is
already “received” wisdom.’37
Apropos to this, it is acknowledged38,39 that nonfunctional-pseudogene beliefs took
hold at a time when the genome was little understood, and when sociobiology
dominated all of biology,40 favouring such attitudes. The classic essays by Orgel,
Crick, Doolittle and Sapienza, which largely inspired the notion that noncoding DNA
is useless, parasitic and ‘selfish’, are recognizably anthropomorphic and
speculative.41 In addition, Howard and Sakamoto40 stress the fact that, majority
opinion notwithstanding, pseudogene-nonfunction beliefs rest largely upon negative
evidence. In stark contrast to Max,6 others are not so sure that we know, even to
this day, what pseudogenes cannot do (see also Abstract):
‘Short interspersed repetitive DNA elements (SINEs) are found in various
eukaryotes* … . We still do not know the biological significance of these elements
and how these elements evolved to the present status.’42
‘Do these elements [LINEs and SINEs] serve a generally useful function or are they
simply “selfish DNA”?’43
‘However, this is not a strong argument, and whether L1* is “selfish” remains to be
determined.’ 44
‘The problem is that generally one does not know whether a pseudogene has any
noncoding phenotypic effect and whether the effect is deleterious or
advantageous.’45
In addition, the ‘few known functional pseudogenes implies few functional
pseudogenes’ thinking, though presented by Max6 as virtual fact, is recognizably no
more than a hypothesis.46 Moreover, this hypothesis is either explicitly or
implicitly rejected by various investigators, who recognize the fact that the
relatively small number of known functional pseudogenes is not at all commensurate
with their overall significance:
‘There are severe limits to our recognition of the roles of mobile elements … the
knowledge of all of the control elements that may be important to genes is still
very restricted. Since mobile elements occur and carry out useful functions in
positions many kilobases from the initiation of transcription even those
significant mobile elements that have been inserted within the last few million
years may not have been principally recognized. Thus it can be argued that 21
examples represent a large number.’47
‘The question then is: which of the hundreds of thousands of Alu inserts are
contributing to the regulation of nearby genes, and which are without significant
effect?’48
Not surprisingly, the perceived rarity of functional pseudogenes has been self-
perpetuating:
‘… given the fact that there are a million Alu elements in the human genome and
there have been no systematic studies to identify which of them have regulatory
functions, it must be only be a matter of time before human-specific Alus are found
to control gene expression (emphasis added).’28
‘Recognizing that Alu repeats might be junk DNA, most researchers chose to study
their mobility and incidental effects on genome structure, as opposed to their
possible function.’49
Other investigators40 have also discussed how low expectations of pseudogene
function have been self-fulfilling.
Apropos to this, it is erroneous to compare overall pseudogene function to a
defendant in a criminal trial pleading innocence because evidence favourable to him
may emerge in the future.6 To begin with, he is actually seeking acquittal as a
result of the current state of evidence.50 Second, evolutionists cite ‘use current
evidence only’ arguments6 selectively, i.e. for pseudogenes, but certainly not for
naturalistic theories for life’s origins, otherwise they would admit the complete
inadequacy of such theories, and acknowledge an external Designer. But a double
standard is followed instead, and we are assured that no Designer is needed
because, ‘Even though today we cannot explain life’s origins mechanistically, one
day we probably will.’
III. Pseudogene deployment: ‘shared mistakes’ between primate genomes?
Do pseudogenes themselves form a nested hierarchy*?
A large fraction of most pseudogenes differ considerably from their paralogous
genes. For instance, a compilation of 65 primate pseudogene sequences,51 totalling
80.6 kb*, indicates that parts of the pseudogene sequences resemble their paralogs
at not much higher than chance levels (50% for two unrelated strands of DNA). Less
than one-third of the 80.6 kb aggregate sequences are 85% similar to their
paralogs, and a very small unspecified fraction of the same reaches 90%. The
authors point out that progressively lower levels of similarity mean progressively
greater ambiguity as to the origins and the timing of the accumulated
pseudogene/gene differences. Taken to its logical conclusion, this means that
‘shared mistake’ arguments cannot even have relevance, let alone validity, for a
large fraction (perhaps the majority) of pseudogenes.
Numerous pseudogenes consist of multiple paralogous copies in each primate genome.
In such cases, ‘shared mistakes’ take on a life of their own. Evolutionists must
essentially ‘shop around’ for the closest match52 in trying to deduce the
orthologous pairings of pseudogenes from primate to primate. This can also occur in
the case of multiple Alu repeats.53 If evolutionary ‘trees’ indicate an anomaly in
which the pseudogenes of distantly-related primates resemble each other more
closely than those of more closely-related primates, this can always be blamed
after-the-fact on either an artefact of the ‘tree’ itself, or on an incorrect
pairing of orthologs.54
Figure 2
Figure 2. A schematic phylogeny illustrating the hierarchical (vowel) and non-

hierarchical (consonant) deployment of ‘shared mistakes’ among five primates. These
‘mistakes’ can be either the orthologous pseudogenes themselves or the variations
of one orthologous pseudogene to another, or both.
Let us now consider those pseudogenes which have only single copies per primate
genome. In doing this, I will adhere to the evolutionary methodology of counting
only shared similarities and dissimilarities each of which simultaneously differs
from that of ‘less derived’ primates.6 Even so, as shown below, while some
pseudogenes appear to be hierarchically shared (as illustrated in Fig. 2) between
primates,6 others definitely are not. Most of the latter are apomorphic*. (C),
however, is an example of phylogenetic discordancy: it occurs in humans and orangs,
but not in any primates of intermediate evolutionary derivation.
Years ago, I had called attention to a pseudogene which was shared by humans and
gorillas but not chimps.55 It has since been alleged that the chimp pseudogene is
lacking because its locus* had been deleted.56 This is an inference which rests on
the assumption that all primates are evolutionarily related, and so any differences
in DNA sequences must be of secondary origin. Other phylogenetic studies may have
ignored missing loci.57 This complication, usually reckoned ‘missing information’,
eventually makes any phylogenetic analysis uninformative.58
Moreover, missing loci cannot come to the rescue of evolutionists in still other
hierarchy-defying instances of pseudogene deployment:
‘These include two of the OR genes (hOR17-7 and OR17-209), which are intact in
human and chimpanzee, but are pseudogenes in gorilla, due to one-base deletions*.
In both cases, the gorilla pseudogenes are accompanied by an intact variant, a
potential case of heterozygosity with one of the alleles being a pseudogene.’59
Other examples of gorilla-only pseudogenes are given below. Otherwise, one OR
pseudogene is human-specific and another set of OR pseudogenes are shared by humans
and chimps but, ironically, are believed to be of independent origin.
Evolutionists can always invoke the ‘gene inactivation occurred after divergence’
claim, after the fact, in such situations, but such thinking is admittedly an
assumption.60 More pointedly, this ad hoc rationalization begs the question about
pseudogenes forming a phylogenetic nested hierarchy in the first place. And it is
far from the only one. Gene conversions* can also be invoked for apomorphic
pseudogenes, as was the case with the human-only BC200-Beta pseudogene.61
In other primates, the deployment of known pseudogenes also often fails to conform
to a nested evolutionary hierarchy. The spider monkey has an apomorphic gamma-
globin pseudogene.62 Elsewhere, seemingly orthologous DRB3 pseudogenes in the
tamarin and titi contain different ‘inactivating mutations’. According to
evolutionary storytelling, once upon a time some genes had come to resemble each
other by convergence* before each one of them had become a pseudogene.63 In still
another example, we encounter an exact reversal of the usual evolutionary
expectation of genes increasingly becoming converted into pseudogenes in
progressively more derived primates.6 Apropos to this, an inferred inactivation of
the theta-1 globin genes exists in the less-derived non-primates (e.g. rabbit) and
in the less-derived galago, but it is the more-derived higher primates that have
functional orthologs instead.64 As a final example, nuclear pseudogenes in the
primate family Cebidae portray a confusing phylogenetic picture, and this is
largely blamed on confounding homoplasies* among the pseudogenes.65
Ironic to those who highlight pseudogenes as an accumulation of ‘shared mistakes’,6
there are evolutionists who are suspicious of pseudogenes as a means of charting
the course of primate evolution:
‘Pseudogenes appear to be subject to virtually no selection and have, therefore,
been used to provide the missing data. However, most pseudogenes are members of
gene families in which frequent exchange of sequences among members may complicate
interpretations of sequence divergence and phylogeny.’66
Finally, to put the ‘shared pseudogenes’ argument in a broader context, note that
evolutionists cannot even agree as to which particular genomic structures can only
be explained by shared evolutionary descent. The mitochrondrial gene order in birds
has been shown to arise independently.67 The MHC complex exhibits considerable
similarities among primates, with most of these genetic motifs believed to predate
the chimp-human divergence.68 Yet, in a major about-face, evolutionists now
recognize that complex MHC genetic motifs can arise independently.63,69 They
currently reckon only 7 of 13 allelic lineages, and only at most a few of the 135
alleles of the DRB1 locus, as predating the human-chimp split.70
Do nested hierarchies characterize interspersed repeats?
Both creationists and evolutionists recognize the fact that the majority of
classical pseudogenes have always been located close to their protein-coding
paralogous genes. But retropseudogenes are believed to have been retrotransposited
at considerable distances from the paralogous parent gene, and only shared
evolutionary ancestry is supposed to be able to account for such coincident
placement in different primates.6 The most numerous retropseudogenes, by far, are
SINEs (especially Alus71) and LINEs (notably L1 elements), each of which number in
the hundreds of thousands72 in the human genome alone. Evolutionists believe that
these elements are periodically inserted during the course of primate evolution
(Fig. 3), and that each such episode generates a unique new family of interspersed
repeats, creating markers suitable for phylogenetic analyses.
There are, however, numerous rationalizations available for dealing with inserted
elements that fail to conform to a nested hierarchy. Contrary to the claim that
successive families of LINEs and SINEs are hierarchically deployed among animals,
there are many instances where clearly intact loci lack the predicted interspersed
element. This occurs between members of different species73 as well as different
orders.74 The rationalization invoked is this: the LINE or SINE element did not
happen to integrate into that part of the host population which eventually survived
into the present.
Figure 3
Figure 3.Idealized and schematic portrayal of successive amplifications (#1, #2 and

#3) of progressively-younger (thicker-dash) families of SINEs. Between episodes of
retroposition, the source gene(s) supposedly accumulate mutations. This causes each
successive ‘printout’ of retroposited SINEs to differ from previous ones by up to
several unique nucleotide substitutions. These nucleotide differences define a new
SINE family. Similar considerations apply to LINE elements, but many of these
elements can indirectly copy themselves.
Evolutionists have long believed that Alu insertion* is an irreversible process;
hence the absence-presence of an Alu at an orthologous site constitutes an ipso
facto primitive-derived polarity. Were a formerly-inserted Alu to undergo
subsequent deletion, this event would supposedly be betrayed by the simultaneous
deletion of some of the flanking sequence*.6 To the contrary, precise excisions of
Alu units can occur: a gorilla-human shared Alu is absent at the orthologous chimp
locus, and an extra 12 bp right Alu-flanking repeat, added to an empty-site
sequence, marks the missing-Alu spot.75
Members of the ‘wrong’ family of inserted repeats can even share particular
orthologous sites. In one instance, an old-family Alu in the gibbon was found to be
situated at the orthologous site of a new-family Alu in gorillas, chimps and
humans.76 The former was then assumed to be a template for the evolution of the
latter. In another instance,77 a modern-family Alu unit was found in humans,
located anomalously at the site expected for an orthologous older-family unit. So a
gene conversion event was conjured up, after the fact, for having supposedly
reconfigured and ‘modernized’ the onetime old Alu family member to make it nearly
identical to a modern human-specific Alu family member.
For the longest time, many evolutionists have argued that the parallel* insertion
of essentially identical retropseudogene units, at the orthologous site in
different animals, is a virtual impossibility. One estimate placed the odds against
such an event at one in many billions.78 Wouldn’t you know it—the same SINE
units,79,80 as well as LINE units,81 have now been discovered independently
emplaced at orthologous sites in different genomes.
For the vast majority of the ostensibly-younger Alus, there can be no question
about their occurrence in a nested hierarchy, as the vast majority of them are
apomorphic.78 Furthermore, the Ya5 Alu family is a showcase of a violated nested
hierarchy. Originally believed to occur only in humans, Ya5 Alu repeats turned up
in chimps,82 and then gorillas. So it was then supposed that the source gene had
generated Ya5 retropseudogenes prior to the human-chimp-gorilla divergence, and so,
in accordance with a nested hierarchy, these ape Ya5 Alus would also be found at
the orthologous sites in humans. But they were not, and this development was thus
explained away:
‘However, it is also remarkable that according to our interpretation, the PV EPL
must have been active at least once in each of the three divergent HCG lineages.’76
Remarkable indeed. We are seriously asked to believe that the PV EPL source gene
became activated independently in all three primates, and many times in two of
them, after their mutual divergence. The plasticity of organic evolution is a sight
to behold!
Of course, the belief that families of interspersed elements form nested
hierarchies is predicated on the belief that the families are factual entities.
But, not only are apomorphic nucleotide substitutions found, but also ones which
appear, disappear, and then reappear again in ostensibly progressively more derived
Alu families.83 The same occurs in L1 families.74 In addition, there are so many
recent L1 families in existence that they have no clear-cut boundaries, and it is
admittedly difficult to sort out the resulting ‘inconsistent pattern of shared
characters’.84 Such blurring also occurs between the older Alu families.85
Earlier, I noted that the molecular ‘clock’ varies considerably from one pseudogene
to another. The same holds for the rate of nucleotide substitutions in Alu units.
The accumulation of what may ironically be called unshared-mistake nucleotide
differences, between orthologous human-chimp Alu elements, differ significantly
from one Alu element to another. Obviously, independent of ‘age’ and degree of
evolutionary relatedness, nucleotide-substitution rates turn out to be governed by
the base composition of the host DNA.86
How certain is the orthologous pairing of retropseudogenes?
Can we really be sure that the same interspersed repeat is located at the identical
location in different primate genomes? Evolutionists commonly believe that
orthologous inserted-element units and orthologous flanking sequences (including
any flanking repeats) can all be unambiguously identified. The actual situation is
not as clear-cut. As discussed below, orthologs are usually far from identical, and
there are features which reduce the distinctiveness of each inserted element from
another.
To begin with, the Alu units themselves, apart from varying in terms of nucleotide
sequence, do not even have to be of equal length to be judged orthologous.78 In
particular, the differences in length of the poly-A tail, between presumably
orthologous Alu units, are often excused on the basis of the vulnerability of
homopolymeric* sequences to episodes of partial deletion after insertion.87 In
addition, the direct repeats* which usually surround each retropseudogene often
have ambiguous boundaries with the Alu unit itself and/or the surrounding flanking
sequence.26 Furthermore, owing to the prevalence of (A+T) upstream of Alu
insertions,88 the direct repeats are also (A+T)-rich, thereby reducing their
capability of differing from their counterparts in unrelated pseudogenes. This
further diminishes the distinctiveness of suspected orthologous pairings.
Now consider flanking sequences. The earlier discussed fact that there is always
some uncertainty in aligning of sequences18 implies that there must always be an
element of doubt if ostensibly orthologous retropseudogenes are really located in
exactly the same position in two or more genomes. In fact, it is acknowledged that
the exact positions of many retroposed elements are uncertain or erroneous.89
Although primers can recognize presumably orthologous retropseudogene sequences
whose flanking regions differ by as much as 25–30%,90 there are no absolute rules
for the minimum degree of similarity required to justify such orthologous
pairings.89 There are even published instances91 of orthologous pairings of LINE
elements being accepted by several teams of investigators and then, upon
reinvestigation, relocated hundreds of bases apart. Orthologous Alus, with
dissimilarities in flanking sequences approaching 30%, are not limited to
distantly-related primates, but are known to occur even in human-chimp comparisons,
with the flanking repeats additionally differing in both base composition and
overall length.87 In severe cases, the flanking regions of prospective orthologs
are so dissimilar to each other that the orthologous pairing itself is doubtful.58
An unavoidable fudge factor is created by matching inexact sequences. There are
even instances where the nucleotide differences in the presumed-orthologous
flanking sequences actually form phylogenetically discordant groupings:
‘Thus, there is a C and an A shared by the gorilla and orangutan; a G shared by the
baboon and rhesus; a C shared by the gorilla and pygmy chimpanzee; and a T shared
by the orangutan and baboon. These examples of shared characters are discordant.
The orangutan cannot have a recent common ancestry with the gorilla and with the
baboon. The shared nucleotides can be interpreted as having arisen independently in
two lineages. This raises the question of how many of such “shared nucleotides”,
that have been used to support common ancestry, have actually arisen independently
in two lineages(emphasis added)?’71
The flanking sequences which surround paralogous and orthologous retropseudogenes,
already imprecisely similar to each other, are evidently not free to differ from
each other in an unconstrained manner. An examination of three paralogous AS
pseudogenes, each of which is compared to its orthologous pseudogene in different
primates, indicates that flanking sequences vary from each other in a very
nonrandom pattern of nucleotide substitutions that recur in parallel.92 This raises
further doubts about the diagnostic uniqueness, in terms of nucleotide sequence, of
each flanking sequence in the genome, as well as the belief that each such sequence
is so unique that it (and its contained retropseudogene) can only be explained by
shared evolutionary ancestry.
IV. Do orthologous pseudogenes have coincidental alterations?
To begin with, most pseudogenes contain multiple, nonunique alterations relative to
their coding paralogs, making it often difficult to declare which one ostensibly
inactivated the original gene.93 Moreover, orthologous primate pseudogenes can have
different ‘inactivating mutations’.63 The fact that some orthologous human-chimp
pseudogenes contain the same stop codon*6 appears impressive until one realizes
that this is often not the case. For instance, a gorilla-specific CYP21 pseudogene
has a stop codon while its indisputably-functional chimp ortholog does not and its
human pseudogene ortholog does—but at a different location in the sequence.94 The
CD8B1 gene provides another example of a gorilla-only stop codon.95 Elsewhere, a
human OR pseudogene has a stop codon while its orthologous chimp pseudogene does
not.96 And, when coincidental stop codons do occur, this is hardly compelling
evidence for ‘shared mistakes’ in view of evidence for parallel nucleotide
substitutions and parallel deletions (discussed later). The latter is relevant to
frameshift-generated stop codons. Finally, we would expect coincidental stop codons
because there are only three possibilities, and even these do not occur at subequal
frequencies in pseudogenes.97
Nucleotide substitutions in pseudogenes, far from qualifying as ‘shared mistakes
within the shared mistakes (pseudogenes)’, often contradict evolutionary schemes.
The alpha-1,3-GT pseudogene, for instance, includes a nucleotide substitution at
position 726 which is uniquely shared by cows, squirrel monkeys and gorillas.98 In
the alpha-1,2-fucosyltransferase pseudogene,99 at position 258, the human and orang
uniquely share a C, while chimp and gorilla uniquely share T. The rat and chimp
uniquely share C at position 55 in the GLO pseudogene.100 Many nucleotide
substitutions in the long Eta-globin pseudogene are either apomorphic or
phylogenetically discordant.101 Orthologous Alu units of even closely related
primates (e.g. humans and chimps) frequently exhibit considerable variance in
nucleotide positions.87
Figure 4
Figure 4.Schematic portrayal of non-corresponding (black) data observed when

nucleotide positions (columns) of orthologous pseudogenes (rows) are aligned.
Indels cause the misalignments.
Indels don’t fare much better, evolutionarily speaking. One can examine the 25,689
bases of the primate Beta-globin cluster (of which nearly half is the Eta-globin
pseudogene) and quickly see that the vast majority of indels in the entire sequence
are apomorphies. Furthermore, there are so many indels in the whole nearly-26 kb
sequence [tabulated elsewhere22] that large ‘holes’ (Fig. 4) exist in the claimed
sequence alignment of primates’ DNA. Still other indels are phylogenetically
discordant. Although these include individual repetitive nucleotides, this fact
must be put in perspective: some form of repetition is prevalent throughout even
coding sequences.102
Elsewhere, a CYP chimp pseudogene has an 8 bp deletion not shared with its orang-
utan, gorilla or human orthologous pseudogenes.94 A TPI chimp pseudogene has a long
insertion* not found in its human orthologous pseudogene,103 while a DRB6 chimp
pseudogene contains two insertions not shared with its human orthologous
pseudogene.104 Not to be outdone, the gorilla ADPRTP1 pseudogene has a 30 bp
duplicated region absent from its human orthologous pseudogene.105 In another
instance, we observe a unique 6-base deletion/substitution sequence in the SHMT
pseudogene undergoing a phylogenetic somersault: it is absent in the (ancestral)
New World monkeys, present in the (more derived) Old World monkeys, and then is
absent once again in the (most highly derived) apes and humans.106
Whether or not they occur only in pseudogenes, numerous molecular ‘shared events’
(mistakes or not), once considered virtually foolproof ‘perfect markers’ of
evolutionary relatedness, have fallen victim to contrary evidence:
‘Nonetheless, almost every new molecular approach to phylogenetic inference has
been ballyhooed as capable of “revolutionizing” the field … . Similar claims have
been made for other kinds of data in the past. For instance, DNA-DNA hybridization
data were once purported to be immune from convergence, but many sources of
convergence have been discovered for this technique. Structural rearrangements of
genomes were thought to be such complex events that convergence was highly
unlikely, but now several examples of convergence in genome rearrangements have
been discovered. Even simple insertions and deletions within coding regions have
been considered to be unlikely to be homoplastic, but numerous examples of
convergence and parallelism of these events are now known. Although individual
nucleotides and amino acids are widely acknowledged to exhibit homoplasy, some
authors have suggested that widespread simultaneous convergence in many nucleotides
is virtually impossible. Nonetheless, examples of such convergence have been
demonstrated in experimental evolution studies.’58
Of course, evolutionists still have faith (sic) in most if not all of these
molecular markers. But they can hardly maintain any longer that common evolutionary
descent is required to explain such things as ‘shared mistakes’.
V. Pseudogene-based phylogenies in the light of other evidence
Autosomal pseudogene sequence:
Phylogeny:
Eta-globin
(Human–Chimp)Gorilla
UO
(Chimp–Gorilla)Human
Alpha-1,2 FT
(Chimp–Gorilla)Human
Alpha-1,3 GT
(Human–Chimp)Gorilla
Table 2. The ambiguous sharing of “shared mistakes”. From Satta et al. (2000)
It has been asserted6 that evolutionary trees constructed on the basis of DNA
similarities ‘agree remarkably well with the evolutionary trees derived earlier
from anatomic similarities’. This statement is egregiously untrue. If anything,
primate phylogenies are in a mess as a result of major contradictions between
molecular and morphological data.57,107,108 Consider some recent craniodental data,
which is very robust, statistically speaking. In a virtual mockery of pseudogene-
based phylogenies (Fig. 2, Table 2), humans branch off first, followed by chimps,
and finally a gorilla-orang clade*.108 (Gibbon was not considered in this study.)
Pseudogene-derived phylogenies are not even consistent with each other (Table 2). A
common rationalization6 would have us believe that any difficulties in resolving
the human-chimp-gorilla trichotomy have no impact on the validity of evolutionary
theory itself. But consider the original prediction:
‘High expectations were placed on molecular methods, when these were first
introduced, as to their power to resolve the trichotomy problem.’107
It is transparent special pleading to exalt molecular methods when they are
predicted to support evolutionary notions, and then turn around and say that they
are no threat to evolutionary theory when they fail! And, regardless of any post
hoc rationalization invoked by the evolutionist to try to discredit it, the prima
facie evidence (Table 2) refutes the claim that pseudogenes qualify as unambiguous
shared mistakes among primates.
Of course, such inconsistencies are not limited to the H-C-G trichotomy. Barriel109
recently compared the previously-discussed Beta-globin data101 with 75
morphological elements, from another study, in order to construct a general primate
phylogeny. The two data sets were found to conflict with each other, and so were
‘reconciled’ by being pooled together. The morphological data alone had placed the
orang-utan as the sister group of the Homo/Pan/Gorilla clade (as in Fig. 2), but
the pooled data displaced orang with the gibbon. In another study,110 Alu sequences
were cited in support of the tarsier as the sister group of the anthropoid apes
(and man), but this was acknowledged to contradict other phylogenies which place
tarsiers elsewhere in the primate evolutionary tree. Overall, primate phylogenies
constructed on the basis of retropseudogenes are not even confirmed by those based
on other retroposons, the latter of which exhibit considerable phylogenetic
conflicts among just themselves.111
Phylogenies based on ‘shared mistakes’ are not, of course, limited to primates, and
the origin of whales has received much attention.6 Yet there are widely divergent
phylogenetic inferences based on different lines of evidence.112 As usual, much
evidence contradicting evolutionary relatedness is disregarded by the standard
attribution to convergence. Apropos to the unconventional hippo-cetacean clade
controversy, we are now in the proverbial situation of an irresistible force (pro:
SINEs) encountering an immovable object (con: very strong skeletal evidence113).
While some evolutionists insist that a favoured line of evidence trumps any
dissenting evidence, other evolutionists warn against making such an assumption.114
All of the myriad problems with ‘convergent’ evolution, both molecular and
morphological, are much too pervasive to be wished away as unimportant. If organic
evolution is science, in the Popperian sense, and therefore subject to potential
falsification, evolutionists must eventually acknowledge the fact that the overall
profusion of divergent and contradictory phylogenies, pertaining to all forms of
life, falsify macroevolution itself.
VI. Shared ‘mistakes’ without plagiarism or common ancestry
How written ‘plagiarized’ errors can arise without plagiarism
Phylogenetically-shared pseudogenes, as ‘shared mistakes’, have been compared to
plagiarized written errors.6 A defendant was convicted of plagiarism by a court
which recognized that, whereas similarity in books’ contents is to be expected from
independently-acting authors writing about the identical topic, the same cannot be
said about exact written errors. But this, of course, assumes the essential random
nature of such errors, with concomitant extreme improbability of independent
duplication. The court in question would have seen things differently had the
‘duplicated’ errors actually been only partly coincident from one book to another,
especially if it was discovered that similar writing errors could arise
independently after all.115 I will show that both considerations are very much
applicable to pseudogenes.
Factors in the parallel deployment of pseudogenes
Figure 5 illustrates a retropseudogene insertion in its genomic context. In
contrast to the assertion that processed pseudogenes are inserted at random
locations into DNA,6 Miyamoto116 concludes that the tacit belief in the randomness
of SINE insertion into the genome is ‘the least convincing assumption’ related to
their role as phylogenetic markers. He cites evidences which show that specific
target-site selection by retroelements is common. Let us develop this further,
examining progressively finer levels of nonrandomness.
To begin with, lengthy Alu-barren intervals of host DNA are much more common than
can be accounted for by a model which assumes constant probability of Alu
insertion.117 It is hardly surprising that the density of Alu repeats, per kb of
host DNA, varies widely according to location in the genome.118 Furthermore, Alu
units often occur in clusters,119 even to the point of aggregating at almost the
same orthologous position in different animals.120They are often found inserted, at
the same spot, into each other.121,122 Evidence that the same site in the same
primate is invaded repeatedly by Alus recognizably indicates that these are
hotspots for Alu insertion,122 and the same holds for L1 insertions.123
Figure 5
Figure 5.Two orthologous loci are illustrated: One (top) lacks a retropseudogene,
and the second (bottom) contains it (gray). Direct repeats are shown in italics.
These, and the flanking sequence, are shown identical for purposes of clarity. Such
is hardly ever the case.
The vast majority of Alus are located in the richest 40% (in terms of G+C) host
DNA,124 and a disproportionate share of these insertions occur into 40–46% G+C host
DNA.125 Both the tail and target regions are strongly enriched in A.126 There
exists an astonishing positive correlation between (G+C) and CG-dimer* levels in
Alus, or CG-dimer islands, and the (G+C) levels in the host DNA.127
The polynucleotide sequences located upstream some 10–20 sites from inserted Alu
repeats and other retropseudogenes, are strongly biased towards certain
hexamers*,128 and the same holds for L1 elements.129
Out of the 1024 (45) possible patterns of pentanucleotides* observed upstream from
Alu repeats, only three of these are by far the most frequent.130 These, and
successive, observations are recognized as evidence suggesting,131 and even
indicating,132 site-specific insertions for retropseudogenes.
There exists a higher level of nonrandomness, one that is largely independent of,
and therefore superimposed upon, the departures from randomness discussed thus far.
Alu units are found concentrated in mitotic hotspots, early-replicating chromosomal
bands, and other genomic locations.133 Moreover, the insertion of both LINEs and
SINEs are believed to be strongly governed by the timing of chromosomal events.134
Locally, SINEs are believed to insert into existing breaks in the host DNA.135
Finally, experimental evidence136,137 demonstrates that there are very specific
cleavage hotspots, for retropseudogene insertion, in bent or coiled DNA. All of
these observations indicate that the widespread independent acquisition of
interspersed elements (including retropseudogenes) is a workable proposition.
Can retropseudogenes be directly acquired by one individual organism from another?
Some6 try to belittle the fact of horizontally-transmitted* genetic information as
much as possible. But the list of known or strongly-suspected instances27 is now
too large to be swept under the rug. Newer examples include the surprising
discovery of SINE elements shared by distantly-related salmonid species,138 as well
as between such evolutionarily-distant creatures as rodents and squids.15 There are
also horizontally-shared LINE elements between vertebrate classes.139
Independently-originating variations within pseudogenes
It is not difficult to envision parallel occurrences of ‘shared mistakes’ because,
as we have seen, coincidences between orthologous pseudogenes of different primates
are, as a whole, very inexact. Also, as shown below, the similarities between
indisputably unrelated pseudogenes is astonishing, and this indicates that only a
limited number of degrees of freedom exist by which any given pseudogene can
potentially differ from its paralogous gene, paralogous pseudogene(s), and/or
orthologous pseudogene(s).
Consider some additional constraints: the DNA ‘alphabet’ consists of only 4 letters
(bases), and the abundances of each nucleotide usually differ significantly from
25%,140 regardless of the etiology of the DNA sequence. Most pseudogenes, in
comparison with their coding paralogs, are enriched in the following order:
A>T>G>C.51 The same holds for Eta-globin pseudogene orthologs that are
‘progressively older’ insofar as they are shared by progressively more kinds of
primates.141 Likewise, the inferred ‘mutational decay’ of AS pseudogenes shows a
striking parallel pattern of nucleotide substitutions in different paralogous AS
pseudogenes.92
Overall, transitional* nucleotide substitutions occur nearly twice as often as
predicted by chance in pseudogenes.142 And, if there is a single base which differs
from a consensus of 4 other orthologs, this nonconforming base is very likely to be
a transition instead of a transversion*.143 Nor are the bases serially independent.
For instance, if its right-side neighbour is G, the nucleotide C is particularly
prone to vary, from pseudogene to pseudogene, as a transition.97 Nucleotide
triplets also occur at strongly nonrandom frequencies.51
As with the example of lightning proved to strike twice, once it is shown that
pseudogene alterations can happen independently but coincidentally, ‘shared
mistakes’ no longer compel shared evolutionary ancestry. Evolutionists try to get
around this by now arguing that genuine synapomorphies* invariably outnumber
convergent ones. In most instances, this is a theory-driven assumption, because:
‘One can never tell whether two taxa share a nucleotide state by descent (homology)
or chance (analogy).’71
More important, the common supposition that convergent molecular events occur too
sporadically or disjointedly to account for the parallel deployment of ‘shared
events’ (mistakes or not), in different organisms, is decisively contradicted by
recent experimental evidence. Independent nucleotide substitutions144 and
indels145,146 can occur in a sufficiently concerted manner to completely obscure
accepted ancestor-descendant relationships.
The following is a rigorous example of evolutionists attempting to screen out the
effects of convergence. This study101 involved an examination of the 17.2 kb
sequence of the Eta-globin pseudogene that is shared by humans, chimps and
gorillas. Among nucleotide substitutions, 12 parallel transitions and 7
transversions unique to human and chimps were found, compared to only 3 total
substitutions exclusively shared by humans and distantly-related monkeys. Assuming
a random distribution of substitutions, statistical analysis indicated that, at
most, 7 of the 12, and 1 of the 7, of the said human-chimp synapomorphies could
have arisen fortuitously. But such results do not compel an evolutionary origin
because:
‘Naturally, these apparent synapomorphies could still have arisen separately under
nonrandom conditions (e.g. if there were selective pressure in two species to
preserve the same change, or a propensity of a nucleotide at a particular position
to mutation in a particular direction). The simplest explanation, however, is that
these changes are actual synapomorphies.’20
Now evolution of humans and chimps from a common ancestor has never been observed;
nonrandom base substitutions and conserved orthologous base positions have
manifested themselves countless times (and examples of both are reported in this
work). So which explanation is simpler? Furthermore, it would take only a very weak
common biasing effect (that is, a tiny deviation from randomness), imposed over
such a long sequence (17.2 kb) to, at minimum, make up the difference between 7 and
12, and between 1 and 7.
Consider some constraints on pseudogene variance imposed by indels. From pooled
data comprising 78 pseudogenes, it is evident that deletions are much more common
than insertions. The size distribution of indels is strongly skewed, with over 50%
of them only one base in length, and relatively few longer than five bases.8,92 The
DNA content deleted from pseudogenes is itself nonrandom, consisting preferentially
of repeated elements within short simple tandem arrays.147
Finally, with so many divergent and contradictory phylogenies in existence, at
least one of them is bound to fortuitously coincide with the broad outlines of
pseudogene deployment, and alteration, among primates. Consider also the following:
‘… the circularity of using inferred phylogenies to infer properties of molecular
evolution that themselves influenced the reconstruction.’144
Alu units and their constrained differences
The repeated independent insertion of seemingly orthologous SINE units is
facilitated by the (previously noted) fact that each SINE unit can potentially
differ by only a very limited degree from another such unit. Were each Alu unit
very different from another such unit, the chance of coincidental similarity in
different primates, without common evolutionary descent, would be extremely small.
Instead, Alus display an average global similarity of 70% to each other,148 and
this rises to 81–98% within each Alu family’s respective consensus sequence.149
A ‘census’ of up-to 290 base positions150 shows that insertions within Alus are
very nonrandom in terms of both the insertion’s position and length. As for
nucleotide substitutions, hardly any of the 290 positions display less than a 70%
preference for a particular base, with most of the remaining ≤30% dominated by one
‘second choice’. In fact, 195 positions are called CONSBI (conserved before
insertion) because fewer than 14% of all Alus deviate from the preferred nucleotide
at these positions.151 About half of the remaining sites (23 pairs, 46 total)
consist of CG doublet hotspots which are prone to mutate frequently and
(phylogenetically) unpredictably from one Alu element to another.83 For this
reason, many investigators disregard these in phylogenetic analyses.
Such exclusion of nucleotides, however, only raises questions about both the
paralogous and orthologous (phylogenetic) significance of the remaining ones. How
do we know that the other so-called informative nucleotide substitutions are not
also hotspots (albeit less extreme ones)? Nucleotide substitutions would then occur
independently in primates in an apparently hierarchical manner, thus creating both
the ‘Alu families’ and Alu-based phylogenies, but without making the hotspot
locations as obvious. The earlier-discussed evidences for concerted parallel
genomic alterations make the foregoing consideration all the more plausible.
Moreover, there is evidence152 that nucleotide substitutions in the L1 during
replication are nonrandom.
VII. Testing evolutionary claims
The factors governing pseudogene deployment and alteration, from primate to
primate, are highly nonrandom. Consequently, assertions about the impossibility of
independent shared ‘mistakes’6 are incorrect (Fig. 6). The only way that this
conclusion could be contradicted would be through the performance of very detailed
statistical tests which would examine all of the relevant factors.
A valid statistical test of retrospseudogenes must, at a minimum, take into account
the following:
Figure 6
Figure 6.Schematic portrayal of the parallel acquisition of (inexact) ‘shared

mistakes’, rendering a common evolutionary ancestry unnecessary.
1. The fundamental overall nonrandomness (i.e. 50% random similarity in bases51)
of the DNA molecule itself.
2. The ubiquitous presence of indels and resulting subjectivity in the alignment
of units.
3. The liberties created by the after-the-fact invocation of missing loci.
4. The several different levels of nonrandomness pertaining to the insertion
points themselves in the genome.
5. The large number of ‘trials’ (for independent ‘orthologous’ insertions)
created by the vast number of known SINE units.
6. The fudge factor created by tolerating varying and often considerable amounts
of sequence differences in the flanking sequences (and flanking repeats) when
accepting them as orthologous.
7. The limited degree by which one SINE unit can differ from another,
8. The nonrandomness of nucleotide substitutions, indels, etc., in the
retropseudogene unit itself.
Considerations 1–3, and 7–8, must likewise be tested in a manner that is relevant
to classical pseudogenes.
Until such tests are performed, and rigorously substantiate the premise that
classical pseudogenes cannot possibly originate from the independent disabling of
orthologous genes in different organisms, and that retropseudogenes cannot be
inserted independently in the same corresponding locations in different primates,
evolutionistic arguments about shared ‘mistakes’6 should not be given credence.
Not enough is yet known about eukaryotic genomes to construct a comprehensive
creationist model of pseudogenes. Nevertheless, the belief that ‘pseudogenes are
unequivocal support for evolution’6 is invalid. New evidence is constantly being
published that weakens or invalidates one or other long-held evolutionistic beliefs
about pseudogenes. Now, more than ever, it is an exciting time to be a creationist
scientist.
Acknowledgements
I thank the following individuals for advice and review: Dr Paul Nelson, Dr Jerry
Bergman, Dr David DeWitt, and Dr Michael Brown.
Glossary
Alu—A category of well-known SINEs. Return to text.
Antisense RNA—RNA which copies the DNA from the reverse direction. Return to text.
Apomorphy—A trait which is unique to the organism in question. It is not shared
with either ‘less derived’ or ‘more derived’ organisms. Return to text.
Base—Denoting the 4 biochemicals (A—Adenine, G—Guanine, C—Cytosine, T—Thymine (U—
Uracil in RNA)) that are part of a nucleotide. The information to code for proteins
can be stored in sequences of bases. Return to text.
bp— Abbreviation for base-pair. Return to text.
Clade—A branching-off point of an organism or closely-related set of organisms
relative to presumably-ancestral organisms. Return to text.
Convergence—The acquisition, by organisms, of shared traits independently (without
having inherited them from a shared evolutionary ancestor). Return to text.
Deletion—The removal of a segment of the DNA sequence followed by reconnection of
the free ends of the molecular ‘chain’. Compare Insertion. Return to text.
Dimer—An association of two Bases. Return to text.
Direct Repeats—That part of the Flanking Sequence which is duplicated prior to the
insertion of the retropseudogene. See Fig. 5. The direct repeats are illustrated in
italics. Return to text.
Eukaryotes—Organisms which have an organized cell nucleus. All living things,
except bacteria and archarbacteria, are eukaryotes. Return to text.
Flanking Sequence—That part of the DNA ‘chain’ which immediately precedes, and
immediately comes after, a retropseudogene. See Fig. 5. Return to text.
Gene Conversion—The process whereby one gene is used as a template to ‘overprint’
another. The latter thereby is forced to resemble the former. Return to text.
Hexamer—A string of six Bases. Return to text.
Homoplasy—Convergence and Parallelism. Return to text.
Homopolymer—A chain of identical bases: AAAAA … , CCCCC … , GGGGG … , or TTTTT … .
Return to text.
Horizontal Transmission—The direct transmission of genetic information from one
living individual to another. Return to text.
Indel—Acronym for Insertion or Deletion. See Fig. 4. Return to text.
Insertion—The addition of a new segment of the DNA sequence followed by
reconnection of the free ends of the molecular ‘chain’. Compare Deletion. Return to
text.
Intergenic—Occuring on the DNA molecule between genes. Return to text.
Interspersed Repeats—A group of genomic elements which occur in great profusion.
Notable interspersed repeats are LINEs and SINEs. Return to text.
kb—Abbreviation for kilobase; 1000 Bases. Return to text.
L1—A group of well-known LINEs. Return to text.
LINE—Long interspersed nuclear element. A group of retropseudogenes that occur in
the hundreds of thousands in the human genome, and which are typically about 7,000
bases long. Return to text.
Locus (Loci)—A specific position on a chromosome. Return to text.
Nested Hierarchy—A series of progressively narrowly-defined subsets which reflect
presumably-increasing evolutionary derivation. For example, a member of the
vertebrates gave rise to mammals, a member of the mammals gave rise to primates,
and a member of the primates gave rise to humans. See Fig. 2 for an ‘advanced’-
primate nested hierarchy. Return to text.
Nucleotide—A compound of a sugar, phosphate and base—DNA and RNA comprise of
nucleotides. Return to text.
Ortholog—Gene and/or pseudogene which is a counterpart to a similar gene and/or
pseudogene in another primate. An ortholog is presumed to be a copy of an ancestral
gene sequence. Refer to Fig. 1. Compare Paralog. Return to text.
Parallelism—The acquisition, by organisms, of shared traits independently (without
having inherited them from a shared evolutionary ancestor). See Fig. 6. Return to
text.
Paralog—Copy of the same gene, pseudogene, etc. within the same organism. See Fig.
1. Compare Ortholog. Return to text.
Pentanucleotide—A chain of five Nucleotides. Return to text.
Phylogen(-ic, -y)—Related to the construction of an evolutionary ‘tree’. Return to
text.
Poly-A—Consisting of many adenine bases in succession: AAAAAAAA … . Return to text.
Poly-A tail—A sequence of adenine bases at the end of an RNA molecule or a
pseudogene. Return to text.
Purine—The Bases adenine (A) and guanine (G). Return to text.
Pyrimidine—The Bases cytosine (C) and thymine (T). Return to text.
Retro- (-element, -poson, -pseudogene)—A (given structure) created by the reverse
transcription (in effect, ‘backfiring’) of RNA back into the host DNA. Return to
text.
SINE—Short interspersed nuclear element. A group of retropseudogenes that occur in
the hundreds of thousands in the human genome, and each of which is typically about
300 bases long. Return to text.
Stop codon—A triplet of Nucleotides which puts a stop to protein synthesis. Return
to text.
Synapomorphy—A trait which is shared by two or more organisms, and which supposedly
is the result of a recent common evolutionary ancestor. Return to text.
Tail—see Poly-A tail. Return to text.
Transition—In the DNA molecule, the replacement of one Purine by another Purine, or
the replacement of one Pyrimidine by another Pyrimidine. Compare Transversion.
Return to text.
Transversion—In the DNA molecule, the replacement of a Purine by a Pyrimidine, or
vice-versa. Compare Transition. Return to text.
References and notes
1. Zuckerkandl, E. and Hennig, W., Tracking heterochromatin, Chromosoma 104:75,
1995.
2. Zuckerkandl, E. et al., Maintenance of function without selection, J.
Molecular Evolution 29:504, 1989.
3. A pseudogene can be likened to a wheel-less automobile. But, as we shall see,
immobility need not imply nonfunction. Throughout this work, I use ‘evolspeak’ for
purposes of clarity. However, I would like to see nonprejudicial language emerge
(e.g. genoid instead of pseudogene, nucleotide variance instead of nucleotide
substitution or inactivating mutation, etc.).
4. Moreira, M.A.M. and Seuanez, H.N., Mitochrondrial pseudogenes and phyletic
relationships of Cebuella and Callithrix (Platyrrhini, Primates), Primates
40(2):353–364, 1999.
5. Gibson, C.J., Pseudogenes and origins, Origins (Loma Linda) 2(2):91–108,
1994. This article is from a scientific creationist viewpoint.
6. Max, E.E., Plagiarized errors and molecular genetics,
<www.ics.uci.edu/pub/bvickers/origins/molecular-genetics.txt>. (Last update: 12
July 1999). Also <www.talkorigins.org/faqs/molgen> (Last update: 6 June 2000). For
years, Max has argued that pseudogenes, as ‘shared mistakes’ between primate
genomes, constitute unequivocal evidence against special creation and for organic
evolution.
7. Esnault, C. et al., Human LINE retrotransposons generate processed
pseudogenes, Nature Genetics 24:363, 2000. It is currently supposed that master
gene(s), rather than retroviruses, reverse-transcribe themselves into the DNA, thus
generating SINEs and LINEs as pseudogenes.
8. Gu, X. and Li, W-H., The size distribution of insertions and deletions in
human and rodent pseudogenes suggests a logarithmic gap penalty for sequence
alignment, J. Molecular Evolution 40:465–469, 1995.
9. Thorne, J.L. and Kishino, H., Freeing phylogenies from artifacts of
alignment, Molecular Biology and Evolution 9(6):1150–1151, 1992.
10. Li, W-H. et al., Pseudogenes as a paradigm of neutral evolution, Nature
292:237, 1981. The authors match a mouse gene with its inferred pseudogene paralog,
disregarding a 30-nucleotide non-corresponding segment, which is blamed on an
insertion.
11. Nishikimi et al., Cloning and chromosomal mapping of the human nonfunctional
gene for L-gulono-gamma-lactone oxidase, J. Biological Chemistry 269(18):13686,
1994.
12. Kondrashov, A.S. and Koonin, E.V., Molecular evolution in the genomic era,
Cell 101(2):128–129, 2000.
13. Cavalier-Smith, T. and Beaton, M.J., The skeletal function of nongenic
nuclear DNA, Genetica 106:3–13, 1999. Of course, no-one is invoking Lamarckianism,
wherein an organism could somehow communicate with its genome and, in this
instance, expel useless DNA on command.
14. Farlow, B., Stuff or nonsense? New Scientist 166(2232):38–41, 2000.
15. Ohshima, K. et al., Several short interspersed repetitive elements (SINEs)
in distant species may have originated from a common ancestral retrovirus, Proc.
Nat. Acad. Sci. USA 90:6260–6264, 1993.
16. Mager, D.L., Endogenous retroviruses provide the primary polyadenylation
signal for two new human genes (HHLA2 and HHLA3), Genomics 59:255, 1999. On the
other hand, the statement that many harmful pseudogenes have existed at one time or
another, but that all but the most recently-originated harmful ones have been
removed from populations by natural selection, is little more than an evolutionary
and long-age supposition.
17. Mighell, A.J., Vertebrate pseudogenes, FEBS Letters 468:113, 2000.
18. Lomax., M.I. et al., Rapid evolution of the human gene for cytochrome C
oxidase subunit IV, Proc. Nat. Acad. Sci. USA 89:5269, 1992.
19. Minghetti, P.P. and Dugaiczyk, A., The emergence of new DNA repeats and the
divergence of primates, Proc. Nat. Acad. Sci. USA 90:1875, 1993.
20. Fitch, D.H.A. et al., The spider monkey eta-globin (pseudo) gene and
surrounding sequences, Genomics 3:237–250, 1988.
21. Ophir, R. and Graur, D., Patterns and rates of indel evolution in processed
pseudogenes from humans and murids, Gene 205:199–201, 1997.
22. Saitou, N. and Ueda, S., Evolutionary rates of insertion and deletion in
noncoding nucleotide sequences of primates, Molecular Biology and Evolution
11(3):504–511, 1994.
23. Freytag, S.O. et al., Molecular structures of human argininosuccinate
synthetase pseudogenes, J. Biological Chemistry 259:3165, 1984. This disparity is
rationalized away by the ad hoc suggestion that the parent gene has mutated after
the pseudogenes had diverged from it. Supposedly, the 19 unique pseudogene
nucleotide substitutions reflect the state of the parent gene prior to the
divergence.
24. One of the authors of this paper will be Dr Paul Nelson, Ph.D. in Philosophy
with emphasis on biology, from the University of Chicago. Nelson is active in the
intelligent design movement.
25. McCarrey, J.R. and Riggs, A.D., Determinator-inhibitor pairs as a mechanism
for threshold setting in development: a possible function for pseudogenes, Proc.
Nat. Acad. Sci. USA 83:679–683, 1986. Pursuing the earlier analogy of the
pseudogene to a wheel-less car, the latter actually has a nontransportation
function (its motor/transmission turns a thresher). The authors have informed me
that no one has as yet tested their theory.
26. Schmid, C.W. and Shen, C-K.J., The evolution of interspersed repetitive DNA
sequences in mammals and other vertebrates; in: Molecular Evolutionary Genetics,
Plenum Press, New York, pp. 332–337, 348–351, 1985.
27. Walkup, L.K., Junk DNA, TJ 14(2):18–30, 2000.
28. Hamdi, K.H., et al., Alu-mediated phylogenetic novelties in gene regulation
and development, J. Molecular Biology 299(4):931–939, 2000.
29. Li, W-H., Molecular Evolution, Sinauer, Massachusetts, USA, p. 347, 1997.
30. Woodmorappe, J., The Mythology of Modern Dating Methods, Institute for
Creation Research, El Cajon, California, p. 3, 1999.
31. Here’s a facetious example: The evolutionist first says that pseudogenes
have no function. When a function is discovered, he zeroes in on the technicality
of the pseudogene being green and says: ‘Function may be applicable to green
pseudogenes, but to no others!’ When, however, function emerges for striped
pseudogenes, the evolutionist changes his tune and says: ‘Well, green pseudogenes
and striped ones have functions, but this doesn’t really mean anything.’ Time goes
on, and a function turns up for polka-dotted pseudogenes. So we now hear:
‘Pseudogenes are functionless, with the minor exception of green, striped and
polka-dotted ones.’ And so on ad infinitum.
32. Max, E., Reply to Wieland, <www.talkorigins.org/faqs/molgen/wieland.html>.
33. Wieland, C., ‘Junk-making’ viruses neutralize an evolutionary argument, TJ
10(3):296–297, 1996.
34. Dimitri, P. and Junakovic, N., Revising the selfish DNA hypothesis, Trends
in Genetics 15(4):123–124, 1999.
35. An example of this would be an inspection of a warehouse wherein 1,000 boxes
of fruit are stored. All 1,000 are declared by the owner to be vermin-free. An
inspector opens 5 boxes, and finds vermin. Following the ATM fallacy, as practiced
by Max6 in relation to pseudogene function, the owner could plead: ‘You have not
shown that the overwhelming majority of boxes (the 995) contain vermin!’ Obviously,
this will not do. A reasonable suspicion now surrounds the remaining 995 boxes and,
short of examining them all, the burden of proof now shifts to the owner to defend
their wholesomeness. In like manner, the discoveries of functional pseudogenes
create a reasonable suspicion about the (allegedly) nonfunctional majority. Short
of an examination of every single pseudogene (even this would likely be
inconclusive), the burden of proof now shifts to those who continue to advocate
overall pseudogene nonfunction.
36. Popper, K.R., The Logic of Scientific Discovery, Basic Books, New York, pp.
87, 315, 1959. In his classic example, the assertion that all ravens are black is
falsified by observing only one white raven. Now consider the popular (but
erroneous) belief that lightning striking twice in one spot is infinitesimally
improbable. How many instances of lightning striking at different localities will
prove this? None—because, as Popper emphasizes, theories are not validated by any
amount of congenial evidence. How many times must lightning strike twice to
disprove this? Exactly one. And, after that, it becomes pointless to demand more
examples, or to quibble about whether lightning could strike the same location
twice or even 20 times. The ATM fallacy allows evolutionists, in essence, to
recognize one tree after another and yet refuse to admit that they are in a forest.
Essentially the same fallacy occurs when evolutionists assert6 that the discovery
of functional pseudogenes does not threaten the supposition that most pseudogenes
are useless. Really!
37. Weiner, A.M., Do all SINEs lead to LINEs? Nature Genetics 24:333, 2000.
38. Makalowski, W., SINEs as a genomic scrap yard; in: The Impact of Short
Interspersed Elements (SINEs) on the Host Genome, R.G. Landes Co., Texas, p. 81,
1995.
39. von Sternberg, R.M. et al., Genome canalization, Genetica 86:216, 1992.
40. Howard, B.H. and Sakamoto, K., Alu interspersed repeats: selfish DNA or a
functional gene family? New Biologist 2:759, 766, 1990.
41. Fedoroff, N.V. Transposable elements, Annals of the New York Academy of
Sciences 870:256, 1999.
42. Tachida, H. and Iizuka, M., A population genetic study of the evolution of
SINEs, Genetics 133:1023, 1993.
43. Gabriel, A., Transposons in the human genome, in: Molecular Biology and
Biotechnology, VCH Publishers, New York, NY, p. 928, 1995.
44. Fanning, T.G. and Singer, M.F., LINE-1: a mammalian transposable element,
Biochimica et Biophysica Acta 910:209, 1987.
45. Petrov, D.A. and Hartl, D.L., Pseudogene evolution and natural selection for
a compact genome, J. Heredity 91:222, 2000. These authors present the intriguing
theory that pseudogenes have position effects on the expression of nearby genes.
46. Panning, B. and Smiley, J.R., Activation of RNA polymerase III transcription
of Human Alu elements by Herpes simplex virus, Virology 202:408, 1994.
47. Britten, R.J., Mobile elements inserted in the distant past have taken on
important functions, Gene 205:181, 1997. His (now too small) list of 21 known
functional mobile insertions includes 7 Alu elements.
48. Piedrafita, E.J. et al., An Alu element in the myeloperoxidase promoter
contains a composite SP1-thyroid hormone-retinoic acid response element, J.
Biological Chemistry 271:14419, 1996.
49. Schmid, C.W. and Rubin, C.M., Alu: What’s the use? in: Makalowski, Ref. 38,
p. 106.
50. Consider this illustrative counter-example: A conviction rests solely on the
results of one forensic technique. Recent evidence proves that it sometimes
implicates innocent people. In the future, this technique will likely be ruled
inadmissible in court. But the defendant is not grasping at some wished-for future
development: he is citing the current state of affairs, which has already created a
reasonable doubt about his guilt, and for which reason he should be acquitted. In
like manner, more than a reasonable doubt already exists about generalized
‘nonfunctional pseudogene’ beliefs.
51. Blake, R.D. et al., The influence of nearest neighbors on the rate and
pattern of spontaneous point mutations, J. Molecular Evolution 34:190–196, 1992.
52. Grewal, P.K. et al., Recent amplification of the human FRG1 gene during
primate evolution, Gene 227:85, 1999. My Figure 1 illustrates only a few
possibilities. Real primate genomes are vastly more complex.
53. Bailey, A.D. et al., Molecular origin of the mosaic sequence arrangements of
higher primate alpha-globin duplication units, Proc. Nat. Acad. Sci. USA 94:5179–
5180, 1997.
54. Collura, R.V. and Stewart, C-B., Insertions and duplications of mtDNA in the
nuclear genomes of Old World monkeys and hominoids, Nature 378:487, 1995.
55. Ueda, S. et al., A truncated immunoglobulin Epsilon-pseudogene is found in
gorilla and man but not in chimpanzee, Proc. Nat. Acad. Sci. USA 82:3712–3713,
1985.
56. Ueda, S. et al., Multiple recombinational events in primate immunoglobulin
epsilon and alpha genes suggest closer relationship of humans to chimpanzees and
gorillas, J. Molecular Evolution 27:77–83, 1988.
57. Revolo, Molecular phylogeny of the hominoids, Molecular Biology and
Evolution 14(3):248–265, 1997.
58. Hillis, D.M., SINEs of the perfect character, Proc. Nat. Acad. Sci. USA
96:9979–9980, 1999. Whenever a significant fraction of loci are missing in a
phylogenetic comparison of several organisms, there is no way to determine whether
the members of the taxa in question ever contained the inserted element. The
hierarchical sharing of certain inserted elements then becomes untestable. As a
result, missing loci unavoidably introduce a fudge factor relative to any
evaluation of ‘shared mistakes’.
59. Sharon, D. et al., Primate evolution of an olfactory receptor cluster:
diversification by gene conversion and recent emergence of pseudogenes, Genomics
61:27–32, 1999. Even though this situation is decided by one-base deletions, it
must be remembered that (as discussed elsewhere) the vast majority of deletions in
pseudogenes are only one base long. In a broader context, the cluster of genes and
pseudogenes which comprise the Olfactory Receptor (OR) cluster do not show
straightforward hierarchical deployment. Various conversion events (including fused
genes and duplicated genes) are each apomorphic to humans and chimps. Two gene
conversion events occur in the same location in monkey chromosomes, and this is
attributed to a hot spot in the genome.
If one examines the overall percentage of the primate OR gene repertoire that is
occupied by pseudogenes, one does observe a crude increase in percentage relative
to increasingly-derived infra-orders of primates. But this crude progression breaks
down as soon as one includes the prosimians. These least-derived primates have a
percent pseudogene content which overlaps that of even the highly-derived
hominoids. Rouquier, S. et al., The olfactory receptor gene repertoire in primates
and mouse, Proc. Nat. Acad. Sci. USA 97:2873, 2000.
60. Qin, Z. et al., The interleukin-6 gene locus seems to be a preferred target
site for retrotransposon integration, Immunogenetics 33:265, 1991.
61. Martignetti, J.A. and Brosius, J., BC200 RNA, Proc. Nat. Acad. Sci. USA
90:11565–11566, 1993. The gene conversion event supposedly created the human-only
pseudogene after the human-chimp split.
62. Fitch, H.A. et al., Duplication of the gamma-globin gene mediated by L1 long
interspersed repetitive elements in an early ancestor of simian primates, Proc.
Nat. Acad. Sci. USA 88:7396–7398, 1991.
63. Kriener, K. et al., Convergent evolution of major histocompatibility
molecules in humans and New World monkeys, Immunogenetics 51:169–178, 2000.
Elsewhere, an even more conspicuous absence of a common set of gene-inactivating
mutations occurs in the delta-globin and psi-etaglobin pseudogenes of the Old World
monkeys. Far from being ‘shared mistakes’, the various ostensibly gene-silencing
frameshifts, deletions, and point mutations are each unique to rhesus, colubus, and
the baboon: Vincent, K.A. and Wilson, A.C. Evolution and transcription of Old World
Monkey globin genes. J. Molecular Biology 207:466, 478, 1989.
64. Kim, J-H. et al., Unique sequence organization and erythroid cell-specific
nuclear factor-binding of mammalian theta-1 globin promoters, Nucleic Acids
Research 17:5687–5691, 1989. This state of affairs is credited to an assumed
inactivation of the theta-1 globin genes early in primate evolution, followed by
the evolutionary divergence of lower and higher primates, and finally the eventual
secondary reactivation of the theta-1 globin genes in the more-derived higher
primates but not in the less-derived lower primates.
65. Vallinoto, M. et al., Mitochrondrial DNA-like sequence in the nuclear genome
of Saguinus (Callitrichinae, Primates), Genetics and Molecular Biology 23:35–42,
2000.
66. Maeda, N. et al., Molecular evolution of intergenic* DNA in higher primates,
Molecular Biology and Evolution 5:2, 1988.
67. Mindell, D.P., Multiple independent origins of mitochondrial gene order in
birds, Proc. Nat. Acad. Sci. USA 95:10693–10697,1998.
68. Woodmorappe, J., Noah’s Ark: A Feasibility Study, Institute for Creation
Research, El Cajon, California, pp. 202–209, 1996.
69. Kawaguchi, H., C4 genes for the chimpanzee, gorilla, and orangutan,
Immunogenetics 35:16–23, 1992b.
70. Bergstrom, T.F. et al., Recent origin of HLA-DRB1 alleles and implications
for human evolution, Nature Genetics 18:237–242, 1998.
71. Hamdi, H. et al., Origin and phylogenetic distribution of Alu DNA repeats,
J. Molecular Biology 289:866–867, 1999.
72. Boeke, J.D., LINEs and Alus—the polyA connection, Nature Genetics 16:7,
1997.
73. Murata, S. et al., Details of retropositional genome dynamics that provide a
rationale for a generic division, Genetics 142:922–923, 1996. In this study, no
less than 70% of orthologous loci were found to be missing.
74. Smit, A.F.A. et al., Ancestral, mammalian-wide subfamilies of LINE-1
repetitive sequences, J. Molecular Biology 246:406–407, 1995.
75. Westhoff, C.M. and Wyllie, D.E., Investigation of the RH locus in gorillas
and chimpanzees, J. Molecular Evolution 42:667–668, 1996.
76. Leeflang, E.P., Phylogenetic isolation of a human Alu flounder [sic] gene,
J. Molecular Evolution 37:563–565, 1993a.
77. Kass, D.H., Gene conversion as a secondary mechanism of short interspersed
element (SINE) evolution, Molecular and Cellular Biology 15:19–25, 1995.
78. Leeflang, E.P. et al., Mobility of short interspersed repeats within the
chimpanzee lineage, J. Molecular Evolution 37:566–568, 1993b.
79. Cantrell, M.A. et al., An ancient retrovirus-like element contains hot spots
for SINE insertion, Genetics (In Review), 2001.
80. Slattery, J.P. et al., Patterns of diversity among SINE elements from three
Y-chromosome genes in carnivores, Molecular Biology and Evolution 17(5):825–829,
2000. Not surprisingly, some evolutionists have challenged these findings.6 But
others have accepted them.
81. Burton, F.H. et al., L1 gene conversion or same-site transposition,
Molecular Biology and Evolution 8(5):609–619, 1991. An alternative interpretation
suggested by the authors is that the L1 insertions are synapomorphic* after all,
but have undergone gene conversion subsequent to their emplacement. In that case,
the absence of this insertion at the locus of an intermediately-derived rodent must
be explained away somehow. The authors have considered precise excision of the L1
unit, or perhaps the presence of the insertion exclusively at a chromosome that did
not last in the population of the intermediately-derived rodent.
82. Leeflang, E.P. et al., Phylogenetic evidence for multiple Alu source genes,
J. Molecular Evolution 35:12–15, 1992. At the time, the Ya5 Alu family was called
PV (Precise Variant), or HS (Human-Specific), which it isn’t.
83. Yang, A.S., The rate of CpG mutation in Alu repetitive elements within the
p53 tumor suppressor gene in the primate germline, J. Molecular Biology 258:240–
250, 1996.
84. Boissinot, S. et al., L1 (LINE-1) retrotransposon evolution and
amplification in recent human history, Molecular Biology and Evolution 17:924,
2000.
85. Batzer, M.A. et al., Standardized nomenclature for Alu repeats, J. Molecular
Evolution 42:4-5, 1996.
86. Filipski, J. et al., Chromosome location-dependent compositional bias of
point mutations in Alu repetitive sequences, J. Molecular Biology 206:564–565,
1989.
87. Sawada, I. et al., Evolution of Alu family repeats since the divergence of
human and chimpanzee, J. Molecular Evolution 22:318–319, 1985.
88. Daniels, G.R. and Deininger, P.L., Integration site preferences of the Alu
family and similar repetitive DNA sequences, Nucleic Acids Research 13:8941–8943,
1985.
89. Jurka, J., Approaches to identification and analysis of interspersed
repetitive DNA sequences; in: Adams, M.D. et al., Automatic DNA Sequencing and
Analysis, Academic Press, London, New York, pp. 295–296, 1994.
90. Shedrock, A.M. and Okada, N., SINE insertions, BioEssays 22:154, 2000.
91. Smit, A.F.A., Structure and Evolution of Mammalian Interspersed Repeats,
Ph.D. Dissertation, University of Southern California, pp. 130–135, 1996.
92. Casane, D. et al., Mutation pattern variation among regions of the primate
genome, J. Molecular Evolution 45:219–221, 1997.
93. Li, W-H., Evolution of duplicate genes and pseudogenes; in: Evolution of
Genes and Proteins, Sinauer Associates, Massachussets, pp. 30–32, 1983.
94. Kawaguchi, H. et al., Evolutionary origin of mutations in the primate
cytochrome P450c21 gene, American J. Human Genetics 50:776–777, 1992a.
95. Delarbre, C. et al., Duplication of the CD8 Beta-chain gene as a marker of
the man-gorilla-chimpanzee clade, Proc. Nat. Acad. Sci. USA 90:7050, 7052, 1993.
96. Glusman, G. et al., Sequence, structure, and evolution of a complete human
olfactory gene cluster, Genomics 63:230, 2000.
97. Bulmer, M., Neighboring base effects on substitution rates in pseudogenes,
Molecular Biology and Evolution 3(4):324–327, 1986. TGA is by far the most commonly
occurring stop codon. Furthermore, out of 64 possible codons in large human genes,
only 18 of these (of which 11 are common) are vulnerable to conversion into a stop
codon by a single nucleotide substitution: Modiano, G., Nonrandom patterns of codon
usage and of nucleotide substitutions in human alpha and beta-globin genes, Proc.
Nat. Acad. Sci. USA 78:1122, 1981. Kimura, M. The Neutral Theory of Molecular
Evolution, Cambridge University Press, pp. 183–185, 1983. When the cited large
human genes are examined for actual abundances of all possible codons, and the
eventual TGA stop codon-bias is taken into account, the limited possibilities for
stop codon occurrence become all the more obvious. Only 2–4% of the individual
codons in use are within one nucleotide substitution of becoming TGA, the majority-
occurring stop codon in human pseudogenes. Of course, since duplicate gene copies
presumably change into pseudogenes, the positions of the 2–4% progenitor codons are
fixed in each copy. Finally, it is acknowledged that identical stop codons
occurring at the same location in potentially-orthologous pseudogenes need not
imply shared evolutionary ancestry. Such is the case with human and sheep P2
pseudogenes, for which coincidental stop codons are believed to be of independent
origins: Medd, S.M. and Walker, J.E., Evolution of the expressed P2 pseudogene and
the origin of the P1 and P2 genes, Biochemical Journal 293:73, 1993.
98. Galili, U. and Swanson, K., Gene sequences suggest inactivation of Alpha-
1,3-galactosyltransferase in catarrhines after the divergence of apes from monkeys,
Proc. Nat. Acad. Sci. USA 88:7403, 1991.
99. (No listed author), Pseudogene for alpha-(1,2)-fucosyltransferase,
<sayer.lab.nig.ac.jp/~silver/apeData/pfut2/pfut2.html>, July 2000.
100. Ohta, Y. and Nishikimi, M., Random nucleotide substitutions in primate
nonfunctional gene for L-gulono-gamma-lactone oxidase, Biochimica et Biophysica
Acta 1472:409, 1999.
101. Bailey et al., Reexamination of the African hominoid trichotomy with
additional sequences from the primate Beta-globin gene cluster, Molecular Phylogeny
and Evolution 1:115–132, 1992. For example, at position 984, a (T) is uniquely
shared by both the species of chimp and the species of distantly related galago. As
for indels, a deletion spanning positions 5098–5101 is shared only by the
phylogenetically-distant orang and spider monkey. This example does not include
anomalous clustering of indels at homopolymeric sites, where independent generation
of indels is a common occurrence.
102. Gusev, V.D. et al., On the complexity measures of genetic sequences,
Bioinformatics 15(2):994, 1999.
103. Craig, L.C. et al., Characterization of the transcription unit and two
processed pseudogenes of chimpanzee triosephosphate isomerase (TPI), Gene 99:225,
1991.
104. Figueroa, F. et al., Primate DRB6 pseudogenes, Immunogenetics 34:335, 1991.
105. Lyn, D. et al., Conservation of sequences between human and gorilla
lineages, Gene 155:243, 1995.
106. Devor, E. et al., Serine hydroxymethyltransferase pseudogene, SHMT-ps1, J.
Experimental Zoology 282:153, 156, 1998. A more flagrant instance of a ‘shared
mistake’ that cannot be the result of common ancestry is as follows: Two HLA genes
and three HLA pseudogenes in the human genome share an identical deletion. Because
a single ancestral gene is unlikely for this motley group of five, a veritable
dance of ad hoc gene conversion events is invoked. We are asked to imagine that the
two genes and three pseudogenes ‘passed on’ the identical deletion to each other,
each time involving only the short segment of the DNA that surrounds the deletion,
and that they accomplished this perhaps several times, Geraghty, D.E. et al.,
Examination of four HLA Class I pseudogenes, J. Immunology 149:1954–1955, 1992.
107. Satta, Y. et al., DNA archives and our nearest relative, Molecular
Phylogenetics and Evolution 14(2):259–275, 2000.
108. Collard, M. and Wood, B., How reliable are human phylogenetic hypotheses?
Proc. Nat. Acad. Sci. USA 97:5003–5006, 2000.
109. Barriel, V., Pan paniscus and hominoid phylogeny, Folia Primatologica
68:50–56, 1997.
110. Zietkiewicz, E. et al., Phylogenetic affinities of tarsier in the context
of primate Alu repeats, Molecular Phylogenetics and Evolution 11(1):77, 1999.
111. Johnson, W.E. and Coffin, J.M., Constructing primate phylogenies from
ancient retrovirus sequences, Proc. Nat. Acad. Sci. USA 96:10254–10260, 1999. In a
complete breakdown of any semblance to an evolutionary nested hierarchy, HERV-K(C4)
is present in the (less derived) Old World monkeys, and in some apes, but is
anomalously absent at the expected loci in the (highly-derived) gorillas and
chimps. For this reason, a gene-conversion rationalization is invoked.
112. O’Leary, M.A., Parsimony analysis of total evidence from extinct and extant
taxa and the Cetacean-Artiodactyl question (Mammalia, Ungulata), Cladistics 15:315–
330, 1999.
113. Luckett, W.P. and Hong, H., Phylogenetic relationships between the orders
Artiodactyla and Cetacea, J. Mammalian Evolution 5:133–143,154–160, 169, 1998.
114. Gura, T., Bones, molecules … or both? Nature 406:230–233, 2000.
115. Obvious examples include: striking adjacent keys (‘r’ vs. ‘t’), inclusion
of commonly-misspelled words, and use of common grammatical errors. Less
intuitively-obvious ones are: typists independently making the same nonadjacent-key
typos owing to typewriter-key mechanics and/or the physiological mechanics of human
fingers; inexperienced printers botching the same long words in the same way;
fatigued writers slipping into very similar written errors owing to common
perceptual and neuromental processes.
116. Miyamoto, M.M., Perfect SINEs of evolutionary history? Current Biology
1999(9):R816, 1999.
117. Moyzis, R.K. et al., The distribution of interspersed repetitive DNA
sequences in the human genome, Genomics 4:276–281, 1989.
118. Beck, S., Evolutionary dynamics of non-coding sequences within the Class II
region of the human MHC, J. Molecular Biology 255:6, 1996.
119. Makalowski, W. et al., Alu sequences in the coding regions of mRNA, Trends
in Genetics 10(6):188, 1994.
120. Lee, Y. et al., Complete genomic sequence and analysis of the prion protein
gene region from three mammalian species, Genome Research 8:1025, 1033, 1998. These
almost-coincident Alus, inserted at the same hotspot region of the genome, may be
understood as ‘near misses’ in the independent orthologous insertions of Alus.
121. Glusman, G. et al., Genome dynamics, polymorphisms, and mutations in a 350
kb human olfactory receptor gene cluster, Mathematical Modelling and Scientific
Computing 9:30–44, 1998.
122. Bailey, A.D. and Shen, C-K.J., Sequential insertion of Alu family repeats
into specific genomic sites of higher primates, Proc. Nat. Acad. Sci. USA 90:7205-
7208, 1993.
123. DeBerardinis, R.J. and Kazazian, H.H., Full-Length L1 elements have arisen
recently in the same 1 kb region of the gorilla and human genomes, J. Molecular
Evolution 47:300, 1998.
124. Smit, A., The origin of interspersed repeats in the human genome, Current
Opinion in Genetics and Development 6:744, 1996.
125. Smit, A., Interspersed repeats and other mementos of transposable elements
in mammalian genomes, Current Opinion in Genetics and Development 9:658, 1999.
126. Jurka, J. and Klonowski, P., Integration of retroposable elements in
mammals: selection of target sites, J. Molecular Evolution 43:689, 1996.
127. Jabbari, K. and Bernardi, G., CpG doublets, CpG islands and Alu repeats in
long human DNA sequences from different isochore families, Gene 224:126–127.
128. Jurka, J., Sequence patterns indicate an enzymatic involvement in
integration of mammalian retroposons, Proc. Nat. Acad. Sci. USA 94:1875, 1997.
129. Cost, G.J. and Boeke, J.D., Targeting of human retrotransposon integration
is directed by the specificity of the L1 endonuclease for regions of unusual DNA
structure, Biochemistry 37:18089–18090, 1998.
130. Toda, Y. et al., Characteristic sequence pattern in the 5- to 20-bp
upstream region of primate Alu elements, J. Molecular Evolution 50:235, 2000.
131. Toda, Y. et al., Sequence patterns observed in 5' flanking regions of
primate Alu elements, Annals of the New York Acad. Sci. 870:372–373, 1999.
132. Laurent, A.M., Site-specific retrotransposition of L1 elements within human
alphoid satellite sequences, Genomics 46:130–131, 1997. The authors consider L1
insertion to be site-specific, requiring a sequence of 2–10 pyrimidines* followed
by 3–7 purines*. This is at least true for insertion into (A+T)-rich sequences.
133. Holmquist, G.P., Chromosome bands, Amer. J. Human Genetics 51:17–37, 1992.
134. Jurka, J. and Kapitonov, V.V., Sectorial mutagenesis by transposable
elements, Genetica 12:4–6, 2000.
135. Wichman, H.A. et al., Transposable elements and the evolution of genome
organization in mammals, Genetica 86:290, 1992.
136. Usdin, K. and Furano, A.V., Insertion of L1 elements into sites that can
form non-B DNA, J. Biological Chemistry 264:20742, 1989.
137. Feng, Q. et al., Human L1 retrotransposon encodes a conserved endonuclease
required for retrotransposition, Cell 87:907–913, 1996.
138. Hamada, M., A newly isolated family of short interspersed repetitive
elements (SINEs) in Coregonid fishes, Genetics 146:363–364, 1995.
139. Kordis, D. and Gubensek, F., Horizontal SINE transfer between vertebrate
classes, Nature Genetics 10:131–132, 1995. The element belongs to the LINE rather
than SINE family. See also: Kordis, D. and Gubenesek, F., Unusual horizontal
transfer of a long interspersed nuclear element between distant vertebrate classes,
Proc. Nat. Acad. Sci. USA 95:10704–10709, 1998.
140. Gojobori, T. et al., Patterns of nucleotide substitution in pseudogenes and
functional genes, J. Molecular Evolution 18:367, 1982.
141. Koop, B.F. et al., Primate Eta-globin DNA sequences and man’s place among
the great apes, Nature 319:236, 1986.
142. Li, W-H. et al., Nonrandomness of point mutation as reflected in nucleotide
substitutions in pseudogenes and its evolutionary implications, J. Molecular
Evolution 21:58, 1984.
143. Goldman, N., Statistical tests of models of DNA substitution, J. Molecular
Evolution 36:189–190, 1993.
144. Bull, J.J. et al., Exceptional convergent evolution in a virus, Genetics
147:1497–1507, 1997.
145. Cunningham, C.W. et al., Parallel molecular evolution of deletions and
nonsense mutations in Bacteriophage T7, Molecular Biology and Evolution 14(1):113–
116, 1997.
146. Broughton, R.E. et al., Conflicting phylogenetic patterns caused by
molecular mechanisms in mitochrondrial DNA sequences, Systematic Biology 47:696–
701, 1998.
147. Graur, D. et al., Deletions in processed pseudogenes accumulate faster in
rodents than in humans, J. Molecular Evolution 28:283, 1989.
148. Shen M.R. et al., Evolution of the master Alu gene(s), J. Molecular
Evolution 33:312, 1991.
149. Jurka, J., Origin and evolution of Alu repetitive elements; in: Makalowski,
Ref. 38, p. 33.
150. Jurka, J. and Milosavljevic, A., Reconstruction and analysis of human Alu
genes, J. Molecular Evolution 32:117–121, 1991.
151. Britten, R.J., Quantitative study of Alu repeated sequences in primate
genomes, in: Makalowski, Ref. 38, pp. 224–229, 1995. It is also interesting to note
that deletions in Alus occur at nonrandom locations (p. 228). This further reduces
the degrees of freedom by which one Alu repeat can diagnostically differ from
another for purpose of orthologous matching.
152. Furano, A.V., The biological properties and evolutionary dynamics of
mammalian LINE-1 retrotransposons, Progress in Nucleic Research and Molecular
Biology 64:282, 2000.
Greater Than 98% Chimp/Human DNA Similarity? Not Any More.
A Common Evolutionary Argument Gets Reevaluated—By Evolutionists Themselves.
by Dr. David A. DeWitt on April 1, 2003
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Originally published in Journal of Creation 17, no 1 (April 2003): 8-10.
Abstract
A new report in the Proceedings of the National Academy of Sciences suggests that
the common value of >98% similarity of DNA between chimp and humans is incorrect.
A new report in the Proceedings of the National Academy of Sciences suggests that
the common value of >98% similarity of DNA between chimp and humans is incorrect.1
Roy Britten, author of the study, puts the figure at about 95% when insertions and
deletions are included. Importantly, there is much more to these studies than
people realize.
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The >98.5% similarity has been misleading because it depends on what is being
compared. There are a number of significant differences that are difficult to
quantify. A review by Gagneux and Varki2 described a list of genetic differences
between humans and the great apes. The differences include ‘cytogenetic
differences, differences in the type and number of repetitive genomic DNA and
transposable elements, abundance and distribution of endogenous retroviruses, the
presence and extent of allelic polymorphisms, specific gene inactivation events,
gene sequence differences, gene duplications, single nucleotide polymorphisms, gene
expression differences, and messenger RNA splicing variations.’3
Specific examples of these differences include:
1. Humans have 23 pairs of chromosomes while chimpanzees have 24.
Evolutionary scientists believe that one of the human chromosomes has been formed
through the fusion of two small chromosomes in the chimp instead of an intrinsic
difference resulting from a separate creation.
2. At the end of each chromosome is a string of repeating DNA sequences
called a telomere. Chimpanzees and other apes have about 23 kilobases (a kilobase
is 1,000 base pairs of DNA) of repeats. Humans are unique among primates with much
shorter telomeres only 10 kilobases long.4
3. While 18 pairs of chromosomes are ‘virtually identical’, chromosomes 4, 9
and 12 show evidence of being ‘remodeled.’5 In other words, the genes and markers
on these chromosomes are not in the same order in the human and chimpanzee. Instead
of ‘being remodeled’ as the evolutionists suggest, these could, logically, also be
intrinsic differences because of a separate creation.
4. The Y chromosome in particular is of a different size and has many markers
that do not line up between the human and chimpanzee.6
5. Scientists have prepared a human-chimpanzee comparative clone map of
chromosome 21 in particular. They observed ‘large, non-random regions of difference
between the two genomes.’ They found a number of regions that ‘might correspond to
insertions that are specific to the human lineage.’7
These types of differences are not generally included in calculations of percent
DNA similarity.
In one of the most extensive studies comparing human and chimp DNA,8 the
researchers compared >19.8 million bases. While this sounds like a lot, it still
represents slightly less than 1% of the genome. They calculated a mean identity of
98.77% or 1.23% differences. However, this, like other studies only considered
substitutions and did not take insertions or deletions into account as the new
study by Britten did. A nucleotide substitution is a mutation where one base (A, G,
C, or T) is replaced with another. An insertion or deletion (indel) is found where
there are nucleotides missing when two sequences are compared.
A
G
T
C
G
T
A
C
C
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A
G
T
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A
C
C
A
G
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A
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Substitution
Insertion/deletion
Figure 1. Comparison between a base substitution and an insertion/deletion.
Two DNA sequences can be compared. If there is a difference in the nucleotides (an
A instead of a G) this is a substitution. In contrast, if there is a nucleotide
base which is missing it is considered an insertion/deletion. It is assumed that a
nucleotide has been inserted into one of the sequences or one has been deleted from
the other. It is often too difficult to determine whether the difference is a
result of an insertion or a deletion and thus it is called an ‘indel’. Indels can
be of virtually any length.
The Britten9 study looked at 779 kilobase pairs to carefully examine differences
between chimpanzees and humans. He found that 1.4% of the bases had been
substituted, which was in agreement with previous studies (98.6% similarity).
However, he found a much larger number of indels. Most of these were only 1 to 4
nucleotides in length, although there were a few that were > 1000 base pairs long.
Surprisingly, the indels added an additional 3.4 % of base pairs that were
different.
While previous studies have focused on base substitutions, they have missed perhaps
the greatest contribution to the genetic differences between chimps and humans.
Missing nucleotides from one or the other appear to account for more than twice the
number of substituted nucleotides. Although the number of substitutions is about
ten times higher than the number of indels, the number of nucleotides involved in
indels is greater. These indels were reported to be equally represented in the
chimp and human sequences. Therefore, the insertions or deletions were not
occurring only in the chimp or only in the human and could also be interpreted as
intrinsic differences.
Will evolution be called into question now that the similarity of chimpanzee and
human DNA has been reduced from >98.5% to ~95%? Probably not. Regardless of whether
the similarity was reduced even below 90%, evolutionists would still believe that
humans and apes shared a common ancestor. Moreover, using percentages hides an
important fact. If 5% of the DNA is different, this amounts to 150,000,000 DNA base
pairs that are different between them!
A number of studies have demonstrated a remarkable similarity in the nuclear DNA
and mtDNA among modern humans. In fact, the DNA sequences for all people are so
similar that scientists generally conclude that there is a ‘recent single origin
for modern humans, with general replacement of archaic populations.’10 To be fair,
the estimates for a date of a ‘most recent common ancestor’ (MRCA) by evolutionists
has this ‘recent single origin’ about 100,000-200,000 years ago, which is not
recent by creationist standards. These estimates have been based on comparisons
with chimpanzees and the assumption of a chimp/human common ancestor approximately
5 million years ago. In contrast, studies that have used pedigrees or generational
mtDNA comparisons11,12,13have yielded a much more recent MRCA—even 6,500 years!14
Research on observable generational mutation events leads to a more recent common
ancestor for humans than phylogenetic estimates that assume a relationship with
chimpanzees. Mutational hotspots are believed to account for this difference.15
However, in both cases, they are relying on uniformitarian principles—that rates
measured in the present can be used to extrapolate the timing of events in the
distant past.
The above examples demonstrate that the conclusions of scientific investigations
can be different depending on how the study is done. Humans and chimps can have 95%
or >98.5% similar DNA depending on which nucleotides are counted and which are
excluded. Modern humans can have a single recent ancestor <10,000 or 100,000-
200,000 years ago depending on whether a relationship with chimpanzees is assumed
and which types of mutations are considered.
Apes Are Our Brothers—Just Ask the Post Office
by Mike Matthews on April 7, 2003
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'Do you realise our DNA is 98.5% identical?’ These are the words in an
advertisement for the first-class stamp in a new series called ‘The secret of
life,’ released by Royal Mail (UK).
Comparative Genetics Stamp
Cracking the Code Stamp
End of Beginning Stamp
Genetic Engineering Stamp
Medical Futures Stamp
“Do you realise our DNA is 98.5% identical?” These are the words in an
advertisement for the first-class stamp (top right) in a new series called “The
secret of life,” released by Royal Mail (UK). The stamps commemorate the 50th
anniversary of Watson and Crick’s discovery of DNA’s structure and recent advances
in human genome research.
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Posters advertising the stamps are plastered all over Post Offices in the UK—even
AiG staff from the US were bombarded with this message during a recent speaking
trip there [see Busy in Britain].
Cartoonist Peter Brookes of the London Times drew the pictures, using humor to make
his message clear. For his first-class stamp, he chose to show the link between
apes and scientists, and label it “comparative genetics.” Obviously, this implies
that one of the most significant outcomes of DNA research is its evidence for human
evolution.
Another stamp in the collection promotes a similar message. According to Royal
Mail’s promotion on its Web site, the stamp titled “The End of the Beginning,”
which shows scientists completing a jigsaw puzzle, “signifies that the discoveries
made so far, and the mapping that continues, present us with the method of finding
the beginning of life (emphasis added).”1
Discrediting “the god hypothesis”
Indeed, the title of the whole series, “The secret of life,” is taken from a famous
quote by one of the discoverers of DNA’s double-helix structure, Francis Crick, who
saw it as a confirmation of evolution and a death knell to religion. (Crick
announced fifty years ago at a pub in Cambridge: “We have discovered the secret of
life.’)
An outspoken atheist, Crick was motivated by a bigger prize than the Nobel
laureate. He openly admits that he has devoted his life to discrediting what he
considers to be the two most powerful “design” arguments for God: chemicals can’t
explain life and chemical processes can’t explain human consciousness. As he
explained to the London Telegraph:
“I went into science because of these religious reasons, there's no doubt about
that. I asked myself what were the two things that appear inexplicable and are used
to support religious beliefs: the difference between living and nonliving things,
and the phenomenon of consciousness.”2
Although Crick’s work with DNA is more widely known than his work on the human
brain,3 both lines of research were intended to confirm the same conclusion: “The
god hypothesis is rather discredited.”
Of course, nobody can deny the significance of Crick’s discovery. In 1953, it was
still a deep mystery how heredity worked—how living things reproduced and
transmitted their characteristics. The discovery of DNA’s structure truly
revolutionized biology, and led to the mammoth Human Genome Project (see Genome
Mania—Deciphering the human genome: what does it mean … ). The potential medical
benefits from this project are truly exciting, as the stamp “Medical futures”
emphasizes.
On the other hand, the belief that DNA research improves our understanding of human
origins is a farce. Although the field of comparative genetics has revealed some
interesting facts about the similarities (and differences) of DNA among different
species, it says nothing about the origin of our DNA or the historical relationship
between species.
Just because we share half our DNA with bananas, doesn’t mean we’re “half a
banana.”4 Similarly, if there were 98% genetic similarity between humans and chimps
wouldn’t mean that we were 98% chimps.5 But in fact, recent evidence indicates that
the genetic similarity is significantly less than this.
The real lesson of DNA
The real, unheralded lesson of the past 50 years of DNA research is the evidence of
an amazing Designer, who made all things, including a marvelously complex,
efficient “information system” for encoding life—something that could not have
arisen by mere time and chance.
DNA obeys the laws of physics and chemistry, but it carries something much more
than that, something which is not known to arise from mere physics and chemistry—
information.6 A car functions according to the physical laws—i.e. there is nothing
“spooky” that makes cars operate. But the physical laws plus time plus chance could
never build a car. The missing ingredient is information—the intelligent purposive
design impressed onto those raw materials.
In the same way, DNA carries the blueprint for living things, which is transmitted
from one generation to the next, like a series of robots programmed to pass on
their programs to other robots. But since observational science has never revealed
any natural process that can create information, i.e. “write the program,” the most
logical conclusion is that the programs themselves, i.e. the information in the
original created kinds, arose from an intelligent mind—the same way programs arise
today.
But don’t expect such an obvious scientific conclusion from a world steeped in
evolutionary rebellion against its Maker.
Footnotes
1. 2003 collection: the secret of life
<www.royalmail.com/portal/default/all/home?shopConsigniaPage=/shop/catalog/
shopDetail&id=prod240003&_requestid=8851>, 25 February 2003.
2. Do our genes reveal the hand of God?
<http://www.telegraph.co.uk/connected/main.jhtml?xml=/connected/2003/03/19/
ecfgod19.xml>, 20 March 2003.
3. The second half of Crick’s life focused on brain research, as he explained
in his 1994 book The Astonishing Hypothesis: The Scientific Search for the Soul,
which claimed, “Your joys and your sorrows, your memories and your ambitions, your
sense of personal identity and free will, are in fact no more that the behavior of
a vast assembly of nerve cells and their associated molecules.”
4. Wieland, C., Furry little humans? Creation 24(3):10–12, 2002.
5. Note that the 98% figure, which gets bandied about in the press, refers to
chimpanzees, not apes, and it has been lowered to about 95%. See Greater Than 98%
Chimp/Human DNA Similarity? Not Any More.
6. I.e. the sequence of symbols with which DNA is constructed. This sequence
is not inherent in the raw chemistry of DNA, but arises from the information in the
parent’s DNA.
Human/Chimp DNA Similarity Continues to Decrease: Counting Indels
by C Nelson on August 1, 2004
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Originally published in Journal of Creation 18, no 2 (August 2004): 37-40.
Abstract
It is conventionally held that humans and chimps differ only very slightly in their
DNA. However, new evidence suggests that the difference might be much more drastic.
Summary
It is conventionally held that humans and chimps differ only very slightly in their
DNA. However, new evidence suggests that the difference might be much more drastic.
Mutations resulting in DNA insertions and deletions cause much of the genetic
difference between the two species, but are typically not included in estimates of
diversity. Moreover, areas of significant similarity are often affected by
selective constraints. An increasing number of functions are also being discovered
for so-called ‘junk DNA’, suggesting similarity in such DNA is not necessarily due
to common descent. Additional research should aid the understanding of such
important data in the debate over origins.
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Creationists have long maintained that the similarity between human and chimp DNA
is not all that it is touted to be. A new study in the Proceedings of the National
Academy of Sciences could help confirm this.
It is widely held that ‘The common chimpanzee (Pan troglodytes) is our closest
relative. Its genome sequence is about 98.8% identical to our own, and we shared a
common ancestor some six million years ago.’1 The assumption that humans diverged
from chimps roughly this long ago also forms the basis of the mitochondrial clock,2
which ‘continues to be widely used to “time” human evolution and population
movements, both ancient and modern.’3 In the popular-level book Genome, Matt Ridley
states that:
‘Apart from the fusion of chromosome 2, visible differences between chimp and human
chromosomes are few and tiny. In thirteen chromosomes no visible differences of any
kind exist. If you select at random any “paragraph” in the chimp genome and compare
it with the comparable “paragraph” in the human genome, you will find very few
“letters” are different: on average, less than two in every hundred. We are, to a
ninety-eight per cent approximation, chimpanzees, and they are, with ninety-eight
per cent confidence limits, human beings. If that does not dent your self-esteem,
consider that chimpanzees are only ninety-seven per cent gorillas; and humans are
also ninety-seven per cent gorillas. In other words we are more chimpanzee-like
than gorillas are.’4
One creationist response to such arguments regarding human/chimp DNA similarity has
been that ‘Chimp DNA has not been anywhere near fully sequenced so that a proper
comparison can be made’,5 and that this evidence is just as easily explained (and
predicted, for that matter) by the concept of a common designer:
‘Since DNA codes for structures and biochemical molecules, we should expect the
most similar creatures to have the most similar DNA. Apes and humans are both
mammals, with similar shapes, so both have similar DNA. We should expect humans to
have more DNA similarities with another mammal like a pig than with a reptile like
a rattlesnake. And this is so. Humans are very different from yeast but they have
some biochemistry in common, so we should expect human DNA to differ more from
yeast DNA than from ape DNA.’6
In a recent article,7 David A. DeWitt cited a study which found that the two
species are only 95% identical when insertions and deletions are considered,8
showing that the estimate of divergence depends mainly on what type of DNA is being
compared. A number of differences between humans and chimps were named that are
difficult to quantify in an estimate of sequence divergence (that is, the
differences in bases between the human and chimp genomes), including shorter
telomeres in humans, a 10% larger chimp genome, and great differences in
chromosomes 4, 9, 12 and the Y chromosome, for example. Indeed, DNA similarity
estimates ‘do not adequately represent fine changes in genome organization.’9
Considering DNA Gaps
Previous estimates of sequence divergence have focused exclusively on base
substitutions in DNA—that is, one base (or one DNA ‘letter’—A, T, C or G) being
replaced with another. The new calculation, resulting in much less sequence
similarity, also includes insertions and deletions, or indels, (occurring when a
base is added or removed, often resulting in what is known as a frameshift
mutation), in addition to base substitutions. The author of the study, Roy J.
Britten, stated:
‘It appears appropriate to me to consider the full length of the gaps in estimating
the interspecies divergence. These stretches of DNA are actually absent from one
and present in the other genome. In the past, indels have often simply been counted
regardless of length and added to the base substitution count, because that is
convenient for phylogenetics.’10
His findings lend support to the idea that much of the failure of DNA to hybridize
between chimps and humans is the result of missing DNA due to indel events. Britten
then became involved in a follow-up paper in which these initial results were
confirmed; in fact, it was found that ‘the 5% human-chimp difference already
published is likely to be an underestimate, possibly by more than a factor of 2.’11
Various types of mutations
Various types of mutations. Much of the difference between human and chimp DNA can
be attributed to insertions and deletions (indels).
Now, Anzai et al. have published a new report in the Proceedings of the National
Academy of Sciences that confirms this statement. In the study, nearly one-half of
the MHC (major histocompatibility complex) region was sequenced, ‘which to date
represents the longest continuous sequence within this species [chimps], our
closest evolutionary relative’, and has been described as a ‘rapidly evolving’ part
of the genome.12 Although it has been held that human/chimp similarity in the MHC
is ‘so great that the alleles must have originated before the supposed chimp/human
evolutionary divergence’,13 the sequence results actually dropped the DNA
similarity estimate down to 86.7%!14 Indeed, the actual difference between the two
species (when counting indels) is greater than 5% by well more than a factor of
two. Not only this, but ‘evolutionists now recognize that complex MHC genetic
motifs can arise independently’ in primates—that is, at least some similarities
that do exist are not attributable to common descent.15
The human genome contains two MHC Class I genes, the MICA and MICB, yet chimpanzees
contain only one gene at this location, the Patr-MIC. According to evolutionary
speculation, a 95-kb deletion occurred between the two human genes, forming the
hybrid chimpanzee gene ~33–44 million years ago, by far predating the commonly held
divergence date between the two species of 6 million years. Because the two ends of
the chimpanzee gene seem to match up with the beginning of the human MICA and end
of the human MICB genes, it may seem reasonable that common ancestry is feasible.
However, even some humans contain a single gene at this location (called the HLA-
B*4801 allele) very similar to the one found in chimps. The study notes that it ‘is
quite intriguing that an equal-sized deletion involving this very same region and
genes (MICA/B) has happened at distinct points in time in several different primate
species’.16 Yet it is also claimed that other such similar changes in DNA structure
cannot be attributed to convergence, but must be due to common ancestry! Clearly,
similar ‘mistakes’ can arise independently in separate species (as expanded upon by
Woodmorappe17). The hypothesis that a Designer would create the same structures for
the same functions seems to explain the data much more easily. As noted by
Woodmorappe,18 strong selective pressures must have existed in order to prevent the
MHC similarities between primates from being scrambled over supposed millions of
years, further weakening the evolutionary scenario.
The Anzai et al. study also mentions a number of differences between humans and
chimps that may be a result of genetic changes in the MHC genes, including the
difference in handling infectious agents such as HIV, hepatitis B and C, and
susceptibility to Plasmodium falciparum. Therefore, the differences observed in
these genes may portray the believed ‘true’ divergence between the two species much
better than previous estimates.
Although these results are interesting, there has been debate over whether or not
indels should be included in sequence divergence estimates. For example, a mutation
called a translocation can occur, in which a segment of DNA breaks off from one
chromosome and is inserted in another. The original Britten study discussed such
rearrangement events briefly and found them to be frequent. Due to the fact that
indel differences were defined as ‘the full length of the gaps’ in the genomes, the
estimates would not be able to consider this kind of mutational change easily.19
New research will hopefully aid in the understanding of changes in genome
organization, and give clues as to how these changes can be included in estimates
of human/chimp similarity.
Difference Between Coding and Noncoding DNA
Other studies have resulted in estimates of similarity higher than 98.6%, also. For
instance, Wildman et al.20 compared ~90 kilobases of human DNA to chimps and found
a similarity of 98.86%, even when counting indels. This is important evidence,
considering that it is in direct opposition to the data presented by Britten and
Anzai et al. However, it must be understood that the various estimates use
different types of DNA. Wildman’s team examined only coding DNA from a number of
genes. Here, non-synonymous changes (those affecting protein structure by changing
the specific amino acid encoded) are subject to purifying selection. This means
that they can be selected against if they have any effect on the function of the
protein.
Similarly, a study of human chromosome 21 (the smallest chromosome in the human
genome) found only 3,003 nucleotide differences in over 400 kilobases. It was shown
that: ‘The differences in coding, promoter, and exon-intron junction regions were
0.51 ± 0.02%, 0.88 ± 0.03%, and 0.85 ± 0.02%, respectively, much lower than the
previously reported 1.23% in genomic regions’,21 with an overall similarity of
99.3%. Within an evolutionary framework, these results would confirm chimps as our
closest relatives. However, this finding seems to contradict the knowledge of a
high substitution rate on chromosome 21, also leading to the conclusion
‘ … that the higher level of similarity observed in the transcript units in this
study is attributable to the presence of purifying natural selection exerted on the
most important functional portions of the genes, including promoters, coding
regions, and intronic regions near the exon-intron boundary.’22
Therefore, high similarity estimates specifically involve regions of coding DNA
that are functionally constrained. The studies by Britten et al. and Anzai et al.
both consider non-coding DNA, which might be less constrained, and therefore more
free to accumulate random mutations. This non-coding DNA thus serves as a more
accurate portrayal of true divergence. Of course, it is very reasonable within the
context of biblical creation that the most similarity should exist where protein
function is vital, since the same proteins would be used for the same structures by
a common Designer.23 It naturally follows that non-coding DNA, being less
constrained, possibly contains more divergence.
Returning to the Anzai et al. study, which found chimps and humans to be 86.7%
similar, a general trend may be noticed with higher similarity in coding regions.
Whereas most ‘non-MHC genes are involved in basic (homeostatic) cellular functions
that require interindividual as well as interspecies homogeneity’, the MHC genes
‘have to constantly adapt themselves to the microbiological habitat of every
species.’ Therefore, purifying selection tends to maintain the structural
conservation of non-MHC genes because of their specific functions. We can conclude
that the 86.7% estimate ‘may be a better representation of whole-genome sequence
similarity between the human and the chimpanzee’ than previous estimates of 98.6%.
Since ‘the major difference between the human and chimpanzee sequences is
overwhelmingly attributable to indels’,24 estimates not including these mutations
ignore a huge source of potential differences. Recent studies have consistently
found indels to be the main source of variation between humans and chimps.25,26,27
It should also be noted, in contrast to examples of high-sequence similarity, that
sequence divergence in certain regions can exceed 20%.28 As noted by DeWitt,
estimates can be ‘misleading because it depends on what is being compared.’29
Junk DNA
Introns are regions of DNA in the genome that do not code for a protein product,
and are therefore assumed to have no function. Because of this, ‘introns in a
particular gene are often compared between organisms, with the base pair
differences seen between their sequences supposedly indicating the degree and time
of divergence since they last shared a common ancestor.’30 Indeed, functionless
introns should be very different in humans and chimps, or even nonexistent, within
the context of biblical creation. However, evidence is mounting that introns are
not, after all, void of function, and the assumption that they were may ‘come to be
a classic story of orthodoxy derailing objective analysis of the facts.’31 Other
forms of ‘junk’ DNA, obviously said to lack function and thus able to mutate at
random, actually contradict evolutionary phylogenies, such as pseudogenes shared by
humans and gorillas but not chimps, the CYP pseudogene being present only in
chimps, and a substitution in the Alpha-1,3GT pseudogene shared by cows, squirrel
monkeys and gorillas. Many substitutions that are shared take place in a non-random
manner, also weakening the explanatory power of common descent.32 Numerous articles
have been published discussing the functions of various alleged forms of ‘junk’
DNA,33,34,35,36,37,38 and it is encouraging to actually see evolutionary journals
awakening to this important fact. The preservation of introns
‘… suggests they do something indispensable. And indeed a large number are
transcribed into varieties of RNA that perform a much wider range of functions than
biologists had imagined possible. Some scientists now suspect that much of what
makes one person, and one species, different from the next are variations in the
gems hidden within our “junk” DNA.’39
Similarities in introns do, therefore, fit the creationist paradigm quite nicely.
DNA Is Not Everything
I suggest that further research is required in order to sort through this evidence,
research that will also find differences inherent within the chimp kind. Indels can
easily be viewed as intrinsic differences between kinds. The DNA sequence is not
all that distinguishes different kinds of organisms—as geneticist Steve Jones was
quoted in Creation as saying, ‘We also share about 50% of our DNA with bananas and
that doesn’t make us half bananas, either from the waist up or the waist down.’40
Evidence has certainly emerged that ‘DNA is not everything’; for example,
mitochondria, ribosomes, the endoplasmic reticulum and the cytosol are passed
unchanged from parent to offspring (save for possible mutations in mtDNA). In fact,
gene expression is itself under the control of the cell.41 Some animals have
undergone extremely dramatic genetic changes, and yet their phenotype has remained
virtually identical.42 Such epigenetic marks ‘can dramatically affect the health
and characteristics of an organism—some are even passed from parent to child—yet
they do not alter the underlying DNA sequence.’43 This evidence lends great support
to reproduction after kinds (Genesis 1:24–25; 1 Corinthians 15:39), as structures
present within parents are preserved in their offspring.
Conclusion
This is an exciting time for creationists as estimates of human/chimp similarity
continue to decrease when indels are considered. Although it is obvious that the
two species are very much alike in the mere DNA sequences (many of the same
structures are present in both, so this would be expected in a creation model), the
previous estimate of ~98.6% sequence identity may have been dealt a significant
blow. Upcoming research will likely shed new light on the many differences between
humans and other animals, and continue to affirm the truth of Genesis.
Acknowledgements
I wish to thank Kim Risely for reviewing an earlier draft of this manuscript. Also,
I recognize Reed Cartwright, David DeWitt and Carl Wieland for providing helpful
information and criticism. I am also indebted to Randy Kim, for having supported,
encouraged and taught me at the times when it was most needed.
About the Author
C.W. Nelson is a high school sophomore with a particular interest in biology as it
relates to evolutionary theory. His first article, concerning the genetic evidence
for the Flood, was published in TJ in 2003. Since that time, he has attended a
number of Creation conferences, including Creation Conference 2003. He often gives
talks at his school’s Fellowship of Christian Athletes, on topics ranging from
Genesis to Christian love. His current research interests involve population
genetics, chemical evolution and Christian friendship.
Chimp Genome Sequence Very Different from Man
by Dr. David A. DeWitt on September 5, 2005
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Last week, in a special issue of Nature devoted to chimpanzees, researchers
reported the initial sequence of the chimpanzee genome.
For many years, evolutionary scientists-and science museums and zoos-have hailed
the chimpanzee as “our closest living relative” and have pointed to the similarity
in DNA sequences between the two as evidence. In most previous studies, they have
announced 98-99% identical DNA.1 However, these were for gene coding regions (such
as the sequence of the cytochrome c protein), which constituted only a very tiny
fraction of the roughly 3 billion DNA base pairs that comprise our genetic
blueprint. Although the full human genome sequence has been available since 2001,
the whole chimpanzee genome has not. Thus, all of the previous work has been based
on only a portion of the total DNA.
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Last week, in a special issue of Nature devoted to chimpanzees, researchers report
the initial sequence of the chimpanzee genome.2 No doubt, this is a stunning
achievement for science: deciphering the entire genetic make-up of the chimpanzee
in just a few years. Researchers called it “the most dramatic confirmation yet” of
Darwin’s theory that man shared a common ancestor with the apes. One headline read,
“Charles Darwin Was Right and Chimp Gene Map Proves It.”3
Researchers claim that there is little genetic difference between us (only 4%).
This is a very strange kind of proof because it is actually double the percentage
difference that has been claimed for years!4 The reality is, no matter what the
percentage difference, whether 2%, 4%, or 10%, they still would have claimed that
Darwin was right.
example, 1.23% of the differences are single base pair substitutions. This doesn’t
sound like much until you realize that it represents ~35 million mutations! But
that is only the beginning, because there are ~40-45 million bases present in
humans and missing from chimps, as well as about the same number present in chimps
that is absent from man. These extra DNA nucleotides are called “insertions” or
“deletions” because they are thought to have been added in or lost from the
sequence. (Substitutions and insertions are compared in Figure 1.) This puts the
total number of DNA differences at about 125 million. However, since the insertions
can be more than one nucleotide long, there are about 40 million separate mutation
events that would separate the two species.
A
G
T
C
G
T
A
C
C
|
|
|
|
|
|
|
|
A
G
T
C
A
T
A
C
C
A
G
T
C
G
T
A
C
C
|
|
|
|
|
|
|
|
A
G
T
C
-
T
A
C
C
Figure 1. Comparison between a base substitution and an insertion/deletion.
Two DNA sequences can be compared. If there is a difference in the nucleotides (an
A instead of a G) this is a substitution. In contrast, if there is a nucleotide
base which is missing it is considered an insertion/deletion. It is assumed that a
nucleotide has been inserted into one of the sequences or one has been deleted from
the other. It is often too difficult to determine whether the difference is a
result of an insertion or a deletion and thus it is called an “indel.” Indels can
be of virtually any length.
To put this number into perspective, a typical page of text might have 4,000
letters and spaces. It would take 10,000 such full pages of text to equal 40
million letters! So the differences between humans and chimpanzees include ~35
million DNA bases that are different, ~45 million in the human that are absent from
the chimp and ~45 million in the chimp that are absent from the human.
the Bible says. Therefore, man and the apes have never had an ancestor in common.
However, assuming they did for the sake of analyzing the argument, then 40 million
separate mutation events would have had to take place and become fixed in the
population in only ~300,000 generations-a problem referred to as “Haldane’s
dilemma.” This problem is exacerbated because the authors acknowledge that most
evolutionary change is due to neutral or random genetic drift. That refers to
change in which natural selection is not operating. Without a selective advantage,
it is difficult to explain how this huge number of mutations could become fixed in
the population. Instead, many of these may actually be intrinsic sequence
differences from the beginning of creation.
Some scientists are surprised at the anatomical, physical and behavioral
differences between man and chimpanzee when they see so much apparent genetic
similarity. With a philosophy that excludes a Creator God, they are forced to
accept similarity as evidence of common ancestry. However, similarity can also be
the result of a common Designer.
It is the differences that make the difference. The most important difference is
that man is created in the image of God.
Dr. DeWitt is the director of the Center for Creation Studies and an associate
professor of biology at Liberty University in Lynchburg, Virginia, USA. His Ph.D.
is in neurosciences from Case Western Reserve University and the focus of his
research is the cell biology of Alzheimer’s disease. Dr. DeWitt was a featured
speaker at July’s “Creation Mega Conference” where one of his presentations was
titled “Image of God or Planet of Apes.” This talk deals with molecular and
anatomical distinctions between man and the apes.
Footnotes
1. David A. DeWitt, “Greater Than 98% Chimp/Human DNA Similarity? Not Any
More.,” Answers in Genesis, April 1, 2003,
https://answersingenesis.org/genetics/dna-similarities/greater-than-98-chimp-human-
dna-similarity-not-any-more/.
2. The Chimpanzee Sequencing and Analysis Consortium, “Initial Sequence of
the Chimpanzee Genome and Comparison with the Human Henome,” Nature 437 (September
1, 2005): 69–87, doi:10.1038/nature04072.
3. “Charles Darwin Was Right and Chimp Gene Map Proves It,” News-
Medical.net, August 31, 2005,
https://www.news-medical.net/news/2005/08/31/12840.aspx.
deletions although this accounts for most of the differences. A study by Roy
to the 4% reported here. See Roy J. Britten, “Divergence Between Samples of
Chimpanzee and Human DNA Sequences Is 5% Counting Indels,” Proceedings National
Academy Science 99, no. 21 (2002): 13633–13635, doi:10.1073/pnas.172510699.
Evolution: Fact or Fiction?
In Utah and elsewhere, it all depends on your presuppositions.
by Dr. Georgia Purdom on February 2, 2006
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In the current controversies about teaching about the origin of life in public
schools, there is a general misunderstanding of the differences between “origin
science” and “operation science."
In Utah, like many other places in America today, a firestorm has erupted over what
can be taught in the state’s public schools concerning evolution.1 The Utah
legislature is currently considering a bill requiring public school teachers to
inform students that the state does not endorse a particular theory of human
origins.
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A writer for the Salt Lake Tribune newspaper declared that scientists believe there
are “no legitimate contenders” (meaning evolution is supreme) and that the debate
concerning evolution is really about how it happened, not that it happened.2
The writer then discussed problems with the definitions of the word “theory” as
understood (or misunderstood) by the general public vs. what scientists say:
“Scientists reserve the word theory for a hypothesis, or idea, that has withstood
rigorous examination to explain something that can be observed” (emphasis added).
Later in the Tribune piece, a scientist is reported as saying that “Science demands
testable explanations for observable occurrences” (emphasis added). The key word in
both quotes is “observed/observable.”
There is a general misunderstanding of the differences between “origin science” and
“operation science.” Origin science is based on events which happened in the past
and are, therefore, not observable today. Operation science, though, is based on
science currently being done in laboratories that is observable today. While it is
true that operation science can help us understand what may have happened in the
past, it is an extrapolation or best guess based on the evidence that we observe
today.
Scientists are biased just like everyone else in that they bring their preconceived
ideas about the past and how life originated into their research. For example, if a
scientist’s presupposition is that God does not exist and that living organisms are
the result of evolution over millions of years, then his interpretations of the
outcome of operation science will seem to support his view of the past. When a
scientist’s presupposition, however, is that God exists and that living organisms
are the result of His creative powers within a six-day period, he can use this to
properly interpret the results of operation science which support the Bible's
claims. Because all scientists are working with the same data, the battle is not
over the evidence but rather the interpretation of that evidence in light of the
scientist's presuppositions. Origins science, because it is not testable, tends to
be more influenced by a scientist's bias, and therefore tends to be more subjective
rather than objective.
Human and chimp similarity?
The Tribune article then touched on the often-cited similarity of the human and
chimp genomes as evidence from operation science that supports the presupposition
of molecules-to-man evolution/millions of years. One University of Utah biologist
who was quoted declared that human/chimp similarity is “absolutely, completely,
totally convincing. It is proof [of evolution].” This is an astonishing statement,
for nothing in science ever proves or disproves a theory. The evidence either
supports or does not support a theory; proof is too strong of a word, and instead
the word support is always preferred. This same scientist then went on to say that,
“Anyone who has examined the evidence can see that the similarities point toward an
ancient common ancestor that links all species.”
I am a scientist, a molecular geneticist, and I have examined the same evidence,
and I believe the similarities point towards a common Designer that created animal
kinds and man.
And how similar are the human and chimp genomes really? The often-quoted numbers of
96–99% similarity are only for regions of the DNA (DNA is the molecule of heredity)
that code for proteins. If a particular protein serves a function in one organism
and the function was needed in another organism, wouldn’t we expect to find the
same protein?
In addition, the remainder of the genome consisting of “junk” DNA and highly
repetitive sequences has not been examined for similarity. Why? Because in the
evolutionists’ mind, they are not important.
“Junk” DNA, for example, is thought of as an evolutionary leftover. However, there
is increasing evidence to support a role for so-called “junk” DNA. It may serve a
role in regulating how much protein is eventually expressed from the DNA. “Junk”
DNA may also serve as a spacer between genes (protein coding sequences) much like
the function of the spaces between the words in this article—without them the
letters wouldn’t make any sense.
Differences between humans and chimps
Here are some other interesting differences between the human and chimp genomes
which are often not reported:
* The chimp genome is 12% larger than the human genome.
* Only 2.4 billion bases have been aligned between the two genomes,
leaving a maximum similarity of 68–77%.
* In many areas of the genome, it appears major rearrangements of DNA
sequences have occurred, accounting for another 10–20% dissimilarity.
* Chimps have 46 chromosomes and humans have 44 chromosomes (excluding sex
chromosomes for both species).
* To save money and time, the chimp genome was assembled using the human
genome as a template (because of the presupposition that humans evolved from the
same line as chimps); it is currently unknown if the pieces of the chimp genome
“puzzle” were put together properly.
To address these concerns and others, comparisons of the human and chimp genomes
will be a part of “GENE” project sponsored by the Institute for Creation Research
(ICR).The bioinformatics team (of which I am a part) will be analyzing different
aspects of the human genome with special emphasis given to the comparison of human
and chimp genomes. As stated by project leader Dan Criswell of ICR, “GENE’s” goal
is “to provide scientific evidence supporting the Biblical position that man was
created distinctly different from the animals, and that each ‘kind’ of animal was
created distinctly different from other ‘kinds’.” Again, it all depends on one’s
presuppositions.
The interpretation of scientific evidence from operation science informs our
beliefs about origin science. What must be understood is that scientists’
presuppositions determine their interpretation of the evidence—God or no God; six
24-hour creation days or evolution/millions of years; accepting the authority of
the Bible or not adhering to the Bible.
A biologist in the Tribune article is quoted as saying, “It’s very difficult to be
a biologist and not recognize the importance of evolution.” I would like to
rephrase that: “It’s very difficult to be a biologist and not recognize the
importance of God and His creation.”
Differences in Gene Expression Distinguish Humans from Other Primates
by Dr. David A. DeWitt on March 20, 2006
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While there is much similarity in DNA sequences and gene expression among them,
there are also important differences. In the case examined, as in other cases, the
differences make the difference.
similarities between humans and the great apes including chimpanzees, gorillas and
orangutans. Over the last few decades, molecular biologists have joined the fray,
pointing out the similarities in DNA sequences. Previous estimates of genetic
similarity between humans and chimpanzees suggested they were 98.5–99% identical.1
However, after the sequencing of the chimpanzee genome last year, the DNA
similarity was fixed at 96%.2 (See Chimp Genome Sequence Very Different from Man.)
Now, a new study highlights important differences that go beyond the DNA sequence.
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Yoay Gilad and colleagues published a paper in the prestigious science journal
Nature in which they report an analysis of differences in gene expression among
humans and other primates.3 Using a cDNA array (cDNA is complementary to mRNA and
provides the exact code for proteins), they examined the expression of 907 genes in
the liver from humans, chimpanzees, orangutans and rhesus macaques. They found a
relatively large number of genes (110) that were expressed at different levels in
humans and chimpanzees. In some cases, humans produce more of a particular gene
product, and in other cases, less. This type of study of gene expression is quite
different from those that investigate DNA sequences. Evolutionists themselves have
suggested that gene regulation may be responsible for key differences between
humans and chimpanzees.4
Chimpanzee
Orangutan
Rhesus macaque
Human
110
128
176
Chimpanzee
-
150
141
Orangutan
-
-
129
Comparison of the number of differentially expressed genes in various
primates. Adapted from Gilad, Y., Oshlack, A., Smyth, G.K., Speed, T.P., and White,
K.P. Expression profiling in primates reveals a rapid evolution of human
transcription factors, Nature 440:242–245, 2006.
While the DNA sequence of a gene specifies the amino acid sequence of the protein,
the expression level is the amount of the protein that is made. In other words, the
DNA sequence spells out the code for producing a specific protein whereas the
expression level is the number of copies that will be produced. The amount of
protein that is produced can make a profound difference, and in some cases a more
important difference than a change in the DNA sequence.
For example, the amount of melanin (dark pigment in the skin) can be altered by the
amount of UV light exposure (the reason people “tan” in the summer). The DNA
sequence that determines the proteins involved in melanin production does not
change, but the amount of those proteins does change. An increase in the amount of
protein can lead to an increase in the amount of melanin.
Often, the amount of a protein that is produced is determined by the functional
equivalent of “thermostats” called transcription factors. Transcription factors are
proteins that bind to DNA just in front of the sequence that codes for a particular
gene. The transcription factors serve as molecular switches to determine whether a
gene is turned on or off, and how much of each to make. Clearly, the control of
gene expression is very important.
Yoay and colleagues compared the level of expression for the 907 gene products
across the various primates. They suggested that the number of differentially
expressed genes followed an evolutionary progression. Humans and chimpanzees
allegedly diverged from a common ancestor 5 million years ago, orangutans 13
million years ago and Rhesus 70 million years ago. Therefore, humans should have
the fewest number of differentially expressed genes with chimpanzees, then
orangutans, and the most with the rhesus macaque.
While that trend is apparent (Table 1), there is a discrepancy. Chimpanzees are
supposed to be more recently related to orangutans than rhesus macaques. However,
chimpanzees have slightly more differentially expressed genes compared to
orangutans than compared to rhesus. In addition, the orangutan has essentially the
same number of differentially expressed genes with humans as with the rhesus
macaques.
Although 60% of the genes had similar expression profiles across the different
species, this still leaves 40% that are altered in at least one species relative to
the others. For example, the researchers found 19 genes that were expressed
differently by humans, but the same in each of the other species. Each species has
certain genes that are expressed at different levels than in the other species.
There may be even more significant differences in gene expression in humans and the
various primates. This study only compared the gene expression in adult livers.
Other organs, especially the brain, are likely to show even more differences in
gene expression than the liver. It is also possible that there are many other
differences in gene expression during development. For example, some genes may be
expressed differently at various times as a baby grows in the womb.
As a creationist, I believe that God made humans, chimpanzees, orangutans and
rhesus macaques separately (but on the sixth day of creation week). While there is
much similarity in DNA sequences and gene expression among them, there are also
important differences. In this, as in other cases, the differences make the
difference.
Visiting the Family?
by Paul F. Taylor on September 5, 2006
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I have a soft spot for Twycross Zoo. It is a favourite with my children and me,
since it is only a 30-minute drive from our house in the west of Leicestershire.
Although much of the information at the zoo is of benefit—their presupposition can
lead visitors to believe in a common ancestor.
The animals seem to be well-looked after, and the atmosphere is friendly and
helpful. Three quarters of the animals in the zoo are endangered species, and so
the zoo runs a well-established captive breeding programme.
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The zoo contains Britain’s largest collection of primates. These are housed in
clean, warm enclosures, with easy access to extensive outdoor apparatus, on which
they can climb and swing. This is clearly beneficial to the animals, as well as
highly entertaining to visitors.
The Twycross chimpanzees were famous throughout the 1970s and 1980s when they
became the stars of a familiar set of TV adverts for a well-known brand of tea. The
actions and mouth movements of the chimps were over-dubbed with human voices. My
own favourite edition of those adverts was a simian recreation of the classic
Laurel and Hardy film The Piano. This series of ads came to an end with the
prevailing view being that it is inappropriate to dress chimps up in human clothes.
Twycross Zoo’s latest publicity leaflet is headed “Catch up with the family.”
Inside the brochure a couple of sentences under the headline “Meet the family” read
...
“Chimpanzees and Baboons (like our friend on the cover) are human’s closest living
relatives, in fact, they share 98% of our DNA.”
Paradoxically, this form of simian political correctness has led to a more
extraordinary and less amusing form of anthropomorphism in the zoo.
(Anthropomorphism is attributing human behaviours to nonhuman things.) The zoo’s
latest publicity leaflet is headed “Come and meet the family”! It is perhaps a
trivial point to make, but none of the enclosures show any evidence for evolution.
The only evolution found is on the notices around the enclosures. Here, the public
is reminded that chimpanzees share 98% of our genes.
Our website has published many articles giving a rational explanation to such
statistics, which are used as a presuppositional smokescreen.1 They are used to
mislead zoo visitors into supposing that it is scientific evidence for evolution,
when an alternative presupposition (ours) would lead visitors to suppose that
chimps and humans share a common designer, not a common ancestor.
Much of the information given in the zoo is of benefit—referring to populations
left in the wild, diet, conservation, and behaviour. The visitor just needs to
observe the animals with a mind open in praise to our Creator, who has made
everything well. When I first visited the zoo, it had been raining, and the giraffe
enclosure contained puddles. If you are fortunate to see the same conditions, just
marvel as you watch the giraffe stoop to drink water, wondering how it could have
evolved the valves that stop the blood from rushing to its head and prevent it from
getting giddy as it raises its head to full height again. Forget the evolutionary
just-so stories and remember your Creator.
Despite the evolutionary propaganda, the zoo is worth a visit. But, if you take
your children, make sure you can talk knowledgeably about the exhibits, being
prepared to give that answer for the “hope that is in you.” With the shortage of
good creationist zoos,2 stock up on good books for you and your children from our
catalogue and then take them to see the live animals at Twycross.

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Chapter 10

What About the Similarity Between Human and Chimp DNA?

Figure 1. The double-stranded DNA molecule forms with an A opposite a T and a G

Figure 5: Comparison between a base substitution and an insertion/deletion. Two DNA

Figure 1. The double-stranded DNA molecule forms with an A opposite a T and a G

Figure 5: Comparison between a base substitution and an insertion/deletion. Two DNA

Acorn Worm Diagram

Finding Adam in the Genome: A BioLogos cover-up?

Illustration courtesy of Jon Seest

According to the Genographic Project’s interpretation of my ancestors, their

Figure 1.Schematic illustration of orthologs and paralogs. A, B, C and D represent

Table 1. Aligned sequences of Cytochrome b and mitochondrial-related pseudogenes.

Figure 2. A schematic phylogeny illustrating the hierarchical (vowel) and non-

Figure 3.Idealized and schematic portrayal of successive amplifications (#1, #2 and

Figure 4.Schematic portrayal of non-corresponding (black) data observed when

Figure 6.Schematic portrayal of the parallel acquisition of (inexact) ‘shared

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