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48 Chapter 3 Extensions to Mendel’s Laws
Figure 3.4 In codominance, F 1 hybrids display the traits Figure 3.2 summarizes the differences between com-
of both parents. (a) A cross between pure-breeding spotted lentils plete dominance, incomplete dominance, and codominance
and pure-breeding dotted lentils produces heterozygotes that are for phenotypes reflected in color variations. Determina-
both spotted and dotted. Each genotype has its own corresponding tions of dominance relationships depend on the phenotype
B
A
phenotype, so the F 2 ratio is 1:2:1. (b) The I and I blood group
A B
alleles are codominant because the red blood cells of an I I that appears in the F 1 generation. With complete domi-
heterozygote have both kinds of sugars at their surface. nance, F 1 progeny look like one of the true-breeding par-
(a) Codominant lentil coat patterns ents. Complete dominance, as we saw in Chapter 2, results
in a 3:1 ratio of phenotypes in the F 2 . With incomplete
dominance, hybrids resemble neither of the parents and
D D
S S
P C C C C thus display neither pure-breeding trait. With codomi-
nance, the phenotypes of both pure-breeding lines show up
Gametes C S C D simultaneously in the F 1 hybrid. Both incomplete domi-
nance and codominance yield 1:2:1 F 2 ratios.
Mendel’s law of segregation still holds
S D
S D
F (all identical) C C C C The dominance relations of a gene’s alleles do not affect
1
the alleles’ transmission. Whether two alternative alleles of
C S C D a single gene show complete dominance, incomplete domi-
F 2 nance, or codominance depends on the kinds of proteins
C S determined by the alleles and the biochemical function of
S S
S D
C C C C those proteins in the cell. These phenotypic dominance
relations, however, have no bearing on the segregation of
C D the alleles during gamete formation.
D D
S D
C C C C As Mendel proposed, cells still carry two copies of
S D
D D
S S
1 C C (spotted) : 2 C C (spotted/dotted) : 1 C C (dotted) each gene, and these copies—a pair of either similar or dis-
similar alleles—segregate during gamete formation. Fertil-
(b) Codominant blood group alleles
ization then restores two alleles to each cell without
Blood Type A B AB reference to whether the alleles are the same or different.
Variations in dominance relations thus do not detract from
Red blood
cell A and B Mendel’s laws of segregation. Rather, they reflect differ-
A sugar B sugar sugars ences in the way gene products control the production of
phenotypes, adding a level of complexity to the tasks of
interpreting the visible results of gene transmission and
inferring genotype from phenotype.
A B
A Gene May Have More Than Two Alleles
B B
A A
P I I I I
Mendel analyzed either-or traits controlled by genes with
two alternative alleles, but for many traits, more than two
alternatives exist. Here, we look at three such traits: human
A B
I I
ABO blood types, lentil seed coat patterns, and human
F 1 AB histocompatibility antigens.
ABO blood types
that protrudes from the red blood cell membrane. Each of If a person with blood type A mates with a person with blood
the alternative alleles encodes a slightly different form of type B, it is possible in some cases for the couple to have a
an enzyme that causes production of a slightly different child that is neither A nor B nor AB, but a fourth blood type
form of the complex sugar. In heterozygous individuals, the called O. The reason? The gene for the ABO blood types has
A
B
A
B
A
red blood cells carry both the I -determined and the I - three alleles: I , I , and i (Fig. 3.5a). Allele I gives rise to
B
determined sugars on their surface, whereas the cells of blood type A by specifying an enzyme that adds sugar A, I
A
homozygous individuals display the products of either I or results in blood type B by specifying an enzyme that adds
B
I alone (Fig. 3.4b). As this example illustrates, when both sugar B; i does not produce a functional sugar-adding en-
B
alleles produce a functional gene product, they are usually zyme. Alleles I and I are both dominant to i, and blood
A
codominant for phenotypes analyzed at the molecular level. type O is therefore a result of homozygosity for allele i.