Dominance Relationships

Mendel’s work demonstrated complete dominance relationship between two different

alleles for each gene pair. As more experiments were conducted, some phenotypes and ratios could
not be explained on the basis of complete dominance. These exceptions did not in any way disprove
Mendel’s principles; rather, they extended and developed them.

Incomplete Dominance or no dominance

In this case, dominance is absent and the progeny does not resemble any of its parents. The
F1s are intermediate between the two plants, e.g., flower in color in Mirabilis jalapa (four o’clock
plant).

P1 and P2: RR (Red) x rr (White)

F1: Rr (Pink)

F2: 1 RR (Red) : 2 Rr (Pink) : 1 rr (White)

Co-dominance

When each allele of a gene is associated with a specific substance, co-dominance will occur
when both substances appear together in the heterozygote, e.g., M-N blood types in man.

Multiple Alleles

It is generally assumed that a gene pair has only two alleles. This condition arises from the
presence of homologous pairs of chromosomes in the diploid organism and each one contains alleles
of the gene pair. However, there are many reported cases where more than two alleles exist in a
gene and are defined as a system of multiple alleles. In the multiple allelic systems, the alleles act
within the same phenotypic range and are called isoalleles. Many such isoalleles have been
discovered, some withing the phenotypic range of an abnormal character, mutant isoalleles, and
some withing the phenotypic range of a wild type, normal isoalleles. A multiple allelic system may,
therefore, be quite complex, including various subsidiary isoallelic systems.

Some examples are ABO blood groups in humans. Landsteiner (1900) classified people into
four groups according to the antigens (agglutins) present in the Red Blood Cells (RBC) and antibodies
(isohemagglitinis) present in the serum. The ABO blood groups are determined by the three alleles
of a single gene: IA, IB, and i. The combination of any two allleles will give four different phenotypes:
Type A, Type B, Type AB, and Type O. A and B represent the carbohydrates present on the surface of
the RBCs. Type A has carbohydrate A, Type B has carbohydrate B, Type AB has both A and B while
Type O has none. The A and B carbohydrates on the surface of RBCs serve as antigens that react with
antibodies. Matching compatible blood group is critical for safe blood transfusion. Agglutination
reactions are routinely done to type RBCs. In typing for ABO antigens, RBCs on the slide are mixed
with antisera (serum antibodies) to the A and B blood-group antigens. If the antigen is present,
agglutination happens forming a visible clump on the slide. Determination of which antigens are
present on the recipient and donor RBCs is the basis for matching blood types for transfusion. If Type
A individual is accidently transfused with blood containing Type B cells, the anti-B isohemagglutinin
will bind to the B blood cells leading to lysis.

ABO blood groupings in man based on the presence of agglutinins and agglutinogens

BLOOD CONTAINS REACTION OF RBC WITH

BLOOD-
Antigens in
GROUP GENOTYPE Serum Antibodies
RBCs Anti-A Anti-B
PHENOTYPE (Isohemagglutinin)
(Agglutinin)
A I AI A; I Ai A Anti-B + -
B IBIB; IBi B Anti-A - +
AB I AI B A; B None + +
O Ii None Anti-A and Anti-B - -
+ stands for agglutination, while - stands for no agglutination

There are many other blood group systems in humans and about half o them are multiple
allelic systems. Haploid organisms also have multiple allelic systems but unlike the diploid organisms
which have two alleles at a time, they only have one allele in every organism.

Lethal Genes

Certain genes can cause the death of an organism. These genes may exert their effect early
in life so that death comes when the embryo is newly formed. In other cases, the embryo may
develop normally for a time and then die at later stages of embryonic development. Lethality may
exist as recessive lethals or dominant lethals.

A second major modification of the classic monohybrid ratios is produce by alleles whose
effect is sufficiently drastic to kill bearers of certain genotypes.

Tay-Sachs disorder in humans.

Infants normally exhibit a “startle response” in which they stiffen their arms and legs upon
hearing a sudden noise. Continuation of this reaction beyond four months old to six months old may
be symptomatic of the Tay-Sachs disorder (juvenile amaurotic idiocy), which is due to homozygosity
for a recessive allele. Homozygous recessives fail to produce an enzyme, hexosaminidase A (hex A),
with the result that a lipid, ganglioside GM 2, accumulates in the brain. Hex A is one of two enzymes
in a sequence of lipid catabolic reactions (the other is hexosaminidase B) and consists of alpha and
beta chains of amino acid residues (polypeptide chains). Tay-Sachs disorder results from a change
(mutation) in the allele responsible for the synthesis of the alpha polypeptide chain. This defect
prevents the production of functional hex A. Mental and motor deterioration rapidly follow the
onset of symptoms, accompanied by paralysis and degeneration of the retina, the latter leading to
blindness. The disorder culminates in death, generally before the age of four years. There is no
treatment. The defective recessive allele responsible is, therefore, termed lethal.
Sickle-cell in humans.

Sickle-cell disorder, involving a pair of incompletely dominant alleles, is particularly

prevalent in blacks in the United States and in certain African peoples. Because the alleles are
incompletely dominant, certain phenotypic ratios occur, differing from those of Tay-Sachs.

The hemoglobin of most persons is of a particular chemical structure and is known as

hemoglobin A (for adult hemoglobin). Many chemical variants of hemoglobin A are found in
relatively small numbers of people; one of these, hemoglobin S, is involved in the sickle-cell disorder.
Alleles responsible for hemoglobin types here are Hb A and HbS. Most persons belong to genotype
HbAHbA. Their erythrocytes contain only hemoglobin A and are biconcave disk-shaped. Persons with
sickle-cell anemia are of the genotype Hb SHbS and are characterized by a collection of symptoms,
chiefly a chronic hemolytic anemia. In the blood of such persons, the erythrocytes under reduced
oxygen tension become distorted and appear sickle-shaped. Sickle-shaped cells not only impede
circulation by blocking capillaries, but also cannot properly perform the function of carrying oxygen
and carbon dioxide to and from the tissues.

In heterozygotes, HbAHbS, some rec cells contain hemoglobin A, others hemoglobin S.

Because both types of hemoglobin are produced, rather than a single intermediate form, this is
another case of codominance. Microscopic examination of heterozygotes’ blood under low oxygen
tension discloses both normal and sickled erythrocytes. Under normal conditions, heterozygotes
manifest none of the severe symptoms of Hb SHbS persons, although they may suffer some periodic
discomfort and even develop anemia after a time at high altitudes. Genotypes and phenotypes in
this disorder are as follows:

HbAHbA normal (hemoglobin A only; no sickling of red cells)

HbAHbS sickle-cell trait (hemoglobins A and S; sickling under reduced oxygen tensions)

HbSHbS sickle-cell anemia (hemoglobin S only; sickling under normal oxygen tension)