Incomplete dominance

Works on problems of heredity have shown that the dominance is not of universal occurrence and there are many examples of incomplete dominance in which the genes of an allelomorphic pair express themselves partially when present together in the hybrid. As a result the heterozygotes (Aa) are phenotypically intermediate between two homozygous types (AA* aa).

For instance, when red snapdragon plants are crossed with white snapdragon plants, all the F₁ hy­brids have pink flowers. This third phenotype results from the heterozygote flowers having less red pigment than the red homozygotes. The breeding of the F₁ hybrids produces F₂ offspring with a phenotypic ratio of 1 red to 2 pink to 1 white. In incomplete dominance we can distinguish the heterozygotes from the two homo­zygous varieties, and the genotypic and phenotypic ratios for the F₂ generation are the same, 1:2:1. The segregation of the red and white alleles in the gametes produced by the pink-flowered plants confirms that the genes for flower color are heritable factors that maintain their identify in the hybrids; that is, inheritance is particulate.

It is incomplete dominance – the kind of inheritance of allelic genes where a cross between organ­isms with two different phenotypes (AA x aa) produces offspring with a third phenotype that is a blending (Aa) of the parental traits. Incomplete dominance is manifested when the interacting enzymes are slightly different in their activity.

In humans, traits with incomplete dominant inheritance are size of nose, salience of lips, size of mouth and eyes, distance between eyes, hair types (straight, wavy) and such hereditary disorders as Friedreich’s ataxia, cystinuria are inherited according to principle of incomplete dominance. For any character, the domi- nant/recessive relationship we observe depends on the level at which we examine phenotype; e.g., con­sider a fatal recessive Tay-Sachs disease, inherited disorder of lipid metabolism when crucial enzyme hexosaminidase does not work properly. Brain cells of Tay-Sachs babies lack a crucial lipid-metabolizing enzyme. Thus, lipids accumulate in the brain, causing the disease symptoms and ultimately leading to death.

At the organism level of normal versus Tay-Sachs phenotype, the Tay-Sachs allele qualifies as a re­cessive (aa).

At the biochemical level,however, we observe intermediate phenotype characteristic of incomplete dominance. The hexosaminidase enzyme deficiency can be detected in heterozygotes who have an activity level of the lipid-metabolizing enzyme that is intermediate between individuals homozygous for the normal allele and individuals with Tay-Sachs disease. Heterozygous individuals are genetically programmed to produce only 40-60% of the normal amount of an enzyme that prevents the disease.