ANTHROPOLOGY 1001, SPRING 2020

FIRST STUDY GUIDE: Suggestions: start with lectures. Read Chapter Study Questions. Not definition of words in
bold type . In textbook, check list of terms in bold at end of each chapter, and study questions.
EVOLUTIONARY THEORY
A. PROLOGUE + INTRODUCTORY LECTURE: WHAT IS ANTHROPOLOGY+ Lab #1
What fields make up the discipline of Anthropology?
What subjects are included in Biological Anthropology?
How do comparative studies of primates and modern people fit into a study of “How humans evolved”?
What is science? Must be testable , hypothesis driven.
What is a hypothesis (a testable explanation for natural phenomena which can be tested, and could potentially be
falsifiable
What is a theory? (A set of generalizations based on hypotheses that have been supported through data from
repeated testing.)
What are empirical data (observable )
What is a null hypothesis?
In an experiment , what is an independent variable? A dependent variable?
What are controlled vs. natural experiments?

B. DARWIN’s REVOLUTION: CHAPTER 1, LABS 1 and 2 Lectures “HISTORY OF EVOLUTIONARY THOUGHT” AND
“DARWIN”S REVOLUTION”
Evolution Before Darwin Darwin’s theory depended on prior recognition that
Earth is not the center of the solar system (Copernicus, Galileo)
Concept of species (Plato, John Ray, Li-shih Chen, Linnaeus
Hierarchical classification (Linnaeus (Kingdom, phylum, class, order, family, Genus Species), Li-Shih Chen,
John Ray (genus and species)
species have changed through time in
behavior/ adaptations,
in morphology = early concept of evolution
(John Ray, Cuvier, Buffon, )
Some species have gone extinct (Cuvier – via catastrophes)
some species are more closely related than others (knowledge of shared anatomy) (Linnaeus, Li-Shih
Chen, Cuvier),
the time span of the earth was long, (Lyell – uniformitarianism, ‘deep time’)
Change is gradual not sudden or catastrophic (Lyell, contra Cuvier)
the environment had something to do with causing species to change (Li-Shih Chen, Buffon, Lamarck –
“inheritance of acquired characteristics”

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What was missing??? Understanding of how the environment affects morphology. How do complex structures
arise? (Have to work with what you start out with, change via a series of steps. ). (Discuss current understanding of
how the first eyes in invertebrates and fishes became complex eyes of terrestrial animals)
Darwin’s Revolution
Darwin’s background: collected beetles, studied medicine (briefly), then divinity, then geology. Botany natural
science
Travelled around South America as the naturalist on the Beagle, stopping at many points around the continent.
Read and took with him: Malthus essay “On population” and Lyell’s Principles of Geology” Captain Fitzroy was a
firm believer in a static created earth.
Malthus – struggle for existence. Species naturally produce more offspring than can survive. Creates struggle for
resources
Lyell: The earth has evolved slowly through vast time, via small changes that can be observed in the present
(uniformitarianism “the present is the key to the past”)

Darwin’s Key Experiences in Development of Theory of Natural Selection

1. Already knew about how artificial breeding and selection of special characteristics by breeders of pigeon,
dogs, etc. could result is a wide variety of descendent populations each with the special characteristics
chosen by different breeders. Artificial selection
2. Observed inherent variability of individuals within wild populations and variation between populations of
same species as he moved around S. America. Concluded new variants were constantly appearing
3. Observed unusual fossils in Argentina and noted their similarity to living creatures of same region.
4. Experienced a catastrophic earthquake in Chile that created some new landscapes and opportunities
5. Visited Galapagos Islands far from mainland. Observed unusual variation between populations of ground
finches (migrants from mainland) across the island chain. All were small and brown, all made similar nests
and laid similar eggs. Clearly closely related. BUT, some had parrot-like beads for cracking large seeds,
some had thin beaks for eating insects, some even emulated woodpeckers by poking holes in trees to fish
out grubs with a cactus spine. Concluded that absence of competing species had allowed them to develop
an unusual range of adaptations.
6. Applied thinking of Malthus on competition to existence of innate variability – concluded some individual
variations made those animals even better best suited to their environment, could outcompete rivals,
survive and leave more offspring, Result: Different environments and opportunities give rise to differing
populations -- Natural selection
7. Problem couldn’t explain where new variation came from and how it was transmitted to offspring.
(Explain how the Grant’s study of finch beaks through time and environmental changes (droughts) proved that
environments select for particular characteristics)
Darwins’ Three Postulates:
1. Ability of population to expand is infinite – ability of environment to support animals is finite
2. Individual differ in morphology, in behavior, in ways that affect ability of each animal to survive and
reproduce.
3. Because these advantageous traits are inherited, they will be more common in subsequent generation.
The favorable variants will increase in next generation, spread through population
Darwin’s Problem: Why don’t the favorable traits eventually blend back into the population and disappear?

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Darwin and Wallace. Why did Darwin publish his theory when he did? Why wasn’t Wallace’s theory as influential
as Darwin’s

C. GENETICS: MENDEL AND MENDELIAN GENETICS, STRUCTURE OF DNA, PROTEIN SYNTHESIS (Chapter 2,
Lab 3, Lectures “Genetics I: Mendelian Inheritance and Genetics”,, “Genetics II: From Genotype to
Phenotype”

Mendel was a student of natural science who dropped out and became a monk. He experimented with
pea plants, creating several lines of plants that bred true for each of 7 particular traits: seed (pea) color
(yellow, green) , pea shape (wrinkled,smooth) and other characteristics: flower color, flower position,
peapod shape, stem length. Chapter 2 and the lecture only dealt with two traits : pea color and pea
shape.He then crossed true-breeding plants with one form of the trait with plants with the other form of
the same trait (e.g. pea color). . In each experiment, he labelled initial plants the F 0 generation and
subsequent ‘filial’ generations F1,2,3 etc..

In every case, the first filial generation (F1) only had one form of the trait. (example, in the pea color
experiment, all the pea plants in the first filial generation of a cross between yellow and green pea plants
had only yellow peas. In the next generation (F2), the other color reappeared in the ratio of 3 yellow to
every 1 green.

Mendel’s conclusions: published in 1866 and ignored

1. Each trait is controlled by only two alternative particles (we would now call these genes and the two
variants alleles). Principle:: Inheritance is particulate
2. One of the two particles is always expressed in the plant (is dominant) when present, the other one
recessive) is not expressed if the dominant one is present. No blending! All the first generations of a
cross between two forms of the same trait express the dominant form but have a hidden recessive
particle. This is the only way to explain how the green peas reappear when both parents are yellow
pea plants. (but are hybrids)
3. Each parent only passes on one of two particles it received from its parents (Principle of segregation)
4. Further experiments were carried out with two different traits, each with two forms, thus starting
with four different true-breeding plants. (yellow smooth, yellow wrinkled, green smooth, green
wrinkled). Here the statistical results showed that the passing on to the F1 generation of the color of
the peas is independent of the transmission of the shape of the peas.(Principle of independent
assortment)

Rediscovered in 1900, understood in terms of newly discovered chromosomes, and different processes of cell
division, mitosis and meiosis.
Chromosomes – 46 in humans, 22 homologous pairs (autosomes), one non-homologous pair –the sex
chromosomes X and Y. This is a homologous pair of two XX’s in females but not in males who have an X.,Y
(different traits on each one). 46 is the diploid number in humans

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Ordinary cell replication by division (mitosis) result in one duplication of the chromosome followed by a cell
division, so that each of the two daughter cells has the same number of chromosomes and the same genetic
material as the parent cell. These are diploid cells, like the parent

Creation of gametes (sperm and egg cells) or meiosis involves one duplication of the chromosomes, followed by
two cell divisions, resulting in 4 daughter cells rather than 2, with each daughter having only half the complement
of chromosomes (haploid cells). A haploid egg and a haploid sperm unite to form a diploid fertilized egg, a zygote
with the 23 paris of chromosomes but in this case, one of each pair is from a different parent, so the combined pair
is different from either parent. It represents a new pattern of genes and accounts for some of the variation Darwin
observed. When the chromosomes line up in pairs, one from each parent, they may exchange pieces (crossing
over) leading to entirely new arrangements of genes of each chromosome. (recombinatiion)

(Practice drawing mitosis and meiosis, showing the difference in the number and form of chromosome divisions.)
Understanding of chromosomes and meiosis explains Mendel’s principles of segregation and independent
assortment. He was lucky that each trait he picked was on a different pair of chromosomes, not on the same pair
of chromosomes, which explains independent assortment. If two traits appear to be passed on together, it is
assumed they are linked on the same chromosome.
Concepts to contrast:
dominant vs recessive, heterozygous vs. homozygous, gene vs. allele, allele vs locus, meiosis vs mitosis,
Other concepts: Punnett squares, linkage, recombination
DNA and genes
Structure of DNA (deoxyribonucleic acid)
DNA – double spiral of phosphates and sugars. Each sugar is linked to one of 4 bases (adenine, thymine, guanine
and cytosine, which in turn is connected via hydrogen bonds to the corresponding base on the other strand. A=T,
C=G. A sequence of bases on the phosphate-sugar ‘backbone’ can be a ‘gene’ that codes for a protein (protein
-coding gene or may instead bond to an area of the chain and determine whether that area codes for anything or
not (regulatory gene) , (Exon = region that codes for a protein, intron = region that includes non-coding sequences
How does DNA code for a protein.
In duplication of chromosomes, a DNA molecule ‘unzips’ (hydrogen bonds break) and the bases on each side
attract and bind corresponding bases (C=G, A=T) and their attached sugars and phosphates from the cell
cytoplasm. Each original strand then links to the new corresponding strand resulting in two DNA molecules
identical to the original one.
Protein coding is more complex
First – the DNA region that codes for the desired protein is unxipped, but instead of attracting a series or
complementary DNA bases, it attracts a series of bases forming a different nucleic acid – ribonucleic acid (RNA) The
main difference is that instead of thymine, RNA has uracil, which attaching to the adenine of the DNA template.
The resulting strand is “messenger RNA” and the process of forming it is called “transcription”. It will be ‘read’ in
‘coodons’ which are pieces of RNA with only 3 bases that each 3 specify a particular amino acid. Non-coding
regions (introns) will be snipped out before the mRNA moves to the cytoplasm to start its work, and the final
coding mRNA molecule will be spliced back together.. The mRNA moves out of the nucleus and binds to a
ribosome. Amino acid molecules in the cytoplasm are each bound to a three-base pair “anticodon” of transfer RNA

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(tRNA) which corresponds to a 3-base pair codon on the mRNA. The mRNA moves across the binding site on the
ribosome one codon at a time, and draws in the transfer RNA anticodon and its attached amino acid. The amino
acids then link together to form a protein.
If often happens that some of the coding exons in the mRNA are left out when the molecule is spliced back
together, so that the mRNA molecule will code for a different protein. Since the codons are ‘read’ three base pairs
at a time, a mistake that drops one base, will cause the entire chain after that base to be read differently, which
may produce a non-functional protein or no protein. There is some redundancy in the code as there are 64
different ways to combine three bases but only 20 amino acids. Often the last letter of the three is irrelevant in
biding to an amino acid.
Regulatory genes determine if a given region is coding for a protein or not. (See glucose-lactose example on p.. 47).
When a protein or enzyme is not needed, a repressor protein binds to the regulatory region, inhibiting
transcription of the protein. When more protein is needed, an activator enzyme will bond to the RNA, increasing
the synthesis of protein at that site..

D. THE MODERN SYNTHESIS, GENES IN POPULATIONS, FORCES OF EVOLUTION, (CHAPTER 3, Lab 4, lectures
“Modern Synthesis: Forces of Evolution and “Formation of Species”
Population Genetics – Hardy-Weinberg Equilibrium
Each reproductive event involves two sets of genes, one from each parent. Hardy-Weinberg provides a way to
understand if the population is biased in some way due to a factor that changes how genes are distributed in the
population.
Mendel worked with peas that had only two different alleles for pea color. In each of his hybrid F 1generations,
each plant had one gene coding for green and on coding for yellow. The frequency of green alleles in the
F1generation is 50% (.50) and the frequency of yellow alleles is also 50% (.50). If the F1 generation mates at
random among themselves, the chances of getting two yellow alleles is .50 x .50 or .25, just as the chances of
getting two heads if you toss enough coins is also 25%, since the frequency of head is 50% and the frequency of
tails is also 50%.
The frequency of a and the frequency of b, if there are only 2 alleles for the trait, must add up to 100%. But
imagine that the you are dealing instead with a gene, for which individuals with two recessive alleles have a serious
disease. Say that in the population of 100, 16 people have the serious disease. (16% of the population) The laws of
probability in random events like which of your offspring get which allele would argue that the frequency of the
bad allele is 40% in the population. If the mother has a 40% chance of passing on the bad gee and the father also
has a 40% chance , the likelihood of getting two bad alleles is .40 time .40. or .16% (of 100). If the frequency of the
bad allele is 40% then 60% of the alleles in the population are good ones. The chances of getting two good ones is
then .6 x .6 or .36 (36% of 100. Finally, what are the chances of having a hidden recessive deleterious gene? Half
the time the mother has a 40% chance of passing on the deleterious gene and the father a 60% chance or vice
versa, the father has the 40% chance and the mother has he 60% chance. 2 x ..40 x .60 is .24 = .48 or 48% of 100
individuals, meaning that 48 individuals have a hidden ‘bad’ gene. 16 (people with the disease). 16 (people with
disease) + 36 (people who are disease-fee and not hybrid) + 48 (individuals with a hidden gene) = 100 individuals.

If you actually could test to see who has a hidden gene (as you can in sickle cell) and instead of getting 48
individuals with a hidden gene you get 64 individuals with a hidden gene, then there is something the population
is doing that is doing that is increasing the percentage of people who have a mixed ancestry (heterozygotes) This
could be due to selection “heterozygote advantage” maybe protects against the disease, , or rules about marrying

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someone who is totally unlike yourself. Either of these are changing the gene pool of the population, which is the
definition of evolution.

The formula is a2+ 2ab + b2, where a if the frequency of the a trait/allele and b is the frequency of the b trait or
allele

Causes of evolution in gene frequencies

Many traits exhibit continuous variation (e.g. height) unlike the traits that Mendel studied.
Continuous variables like height often are controlled by more than one gene
How is variation maintained?
No blending of traits
Mutation adds new variants
Some variation is hidden and not susceptible to selection
Behavioral plasticity – males have a strategy to increase reproduction success.
What keeps some traits from becoming fully adaptive.??
Correlated characters
Disequilibrium
Genetic drift
Constraints of body shape and size on the form of bones and thermoregulation

FORMATION OF SPECIES AND RECONSTRUCTING PHYLOGENIES

Microevolution/macroevolution
Species concepts:
Biological – reproductive isolation
Ecological – different niches, maintained by selection, different reproductive behaviors, etc.
What keep species apart? Isolating mechanisms.-- Can be geographical (speciation on different sides of a physical
barrier
Can be temporal (feed at different times of day) or spatial (feed in treetops vs on the ground)in terms of feeding,
or nesting -- “potential mates do not meet”
Can be mechanical “potential mates cannot mate
Or chemical (egg and sperm from two species are incompatible) or embryo is not viable
Or post -mating – offspring is sterile
Where do species form?

Allopatric – different sides of a barrier

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Parapatric – different environments within the geographic range. Populations become adapted differently to the
different part of the range and separate
Sympatric – strong selection for different phenotypes
Classification and Phylogeny
Based on similarities but some similarities can be due to parallel development of to retention of ancestral traits.
Principle – same trait unlikely to evolve multiple times -- did knuckle-walking evolve twice -- in chimps and gorillas
BUT – some problems due to convergence of an adaptation of a trait
Some problems due to retention of ancestral characters
SOLUTION – use ontogeny (appearance of different traits during growth). ‘recapitulates phylogeny? Teils in
humans and ape embryos
SOLUTION – use genetic distance data compare two similar gene sequences in two species to determine similarity
of genomes, and hence time since last common ancestor. Changes at a more-or-less constant ate

Solution – Cladistics, use only shared derived traits, not ancestral ones.

E. Human Variation. CHAPTER 14, Lab 5, Lectures “Human Variation and Adaptation ”
Humans are not very variable genetically compared to apes
1.2% difference from chimpanzees, 1.3% with bonobos, 1.75b% human and gorillas
71% of the proteins the genes code for are different.
Some nucleotide differences/substitutions do not produce any change in the amino acid sequence
Most of differences between us and apes are due to ??regulatory genes?

Some positively selected genes in us

Form of Fox P2
Look at most different regions of genome?
Genetic variation vs environmental variation?
Sickle ccell anemia and environment

G6PD as another malaria resistance allele

Distribution of lactose resistance. -- paralellism
Morphology – skin color and bone development, cancer susceptibility, immune disorder.

Race as a culturally constructed category -- characteristics vary within populations more than between them
Clinal and geographical correlates of some traits

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Skin color
Distal limb length – talk thin bodies repel heat more easily (Allen’s Rule).
Hair form
Height and stockiness of body 9squarish bodies retain heat better (Bergmann’s rule)

REMEMBER TO CHECK VOCABULARY AND STUDY QUESTIONS AT ENDS OF CHAPTERS AND LECTURE FILES