What is Incomplete Dominance? (With Examples)

The incomplete dominance it is the genetic phenomenon in which the dominant allele does not mask the effect of the recessive allele completely; that is, it is not completely dominant. It is also known as semi-dominance, a name that clearly describes what happens in alleles.

Before its discovery, what had been observed was the complete dominance of the characters in the offspring. The incomplete dominance was described for the first time in 1905 by the German botanist Carl Correns, in his studies of the color of the flowers of the species Mirabilis jalapa.

Intermediate phenotype in F1 generation caused by incomplete dominance

The effect of incomplete dominance becomes evident when the heterozygous descendants of a cross between homozygotes are observed.

In this case, the descendants have an intermediate phenotype to that of the parents and not the dominant phenotype, which is what is observed in cases where dominance is complete.

In genetics, dominance refers to the property of a gene (or allele) in relation to other genes or alleles. An allele shows dominance when it suppresses the expression or dominates the effects of the recessive allele. There are several forms of dominance: complete dominance, incomplete dominance and codominance.

In incomplete dominance, the aspect of the descendants is the result of the partial influence of both alleles or genes. Incomplete dominance occurs in the polygenic inheritance (many genes) of traits such as the color of eyes, flowers and skin.

Examples

There are several cases of incomplete dominance in nature. However, in some cases it is necessary to change the point of view (complete organism, molecular level, etc.) in order to identify the effects of this phenomenon. Here are some examples:

The flowers of the Correns experiment ( Mirabilis jalapa )

The botanist Correns made an experiment with flowers of the plant commonly called dondiego at night, which has varieties of flowers completely red or completely white.

Correns made crosses between homozygous plants of red color and homozygous plants of white color; the offspring presented an intermediate phenotype to that of the parents (pink color). The wild-type allele for the color of the red flower is designated (RR) and the white allele is (rr). A) Yes:

Parental generation (P): RR (red flowers) x rr (white flowers).

Filial generation 1 (F1): Rr (pink flowers).

By allowing these F1 descendants to self-fertilize, the next generation (F2) produced 1/4 of plants with red flowers, 1/2 of plants with pink flowers and 1/4 of plants with white flowers. The pink plants in the F2 generation were heterozygous with intermediate phenotype.

Thus, generation F2 showed a phenotypic ratio of 1: 2: 1, which was different from the phenotypic ratio 3: 1 observed for simple Mendelian inheritance.

What happens in the molecular domain is that the allele that causes a white phenotype results in the lack of a functional protein, required for pigmentation.

Depending on the effects of genetic regulation, heterozygotes can produce only 50% of the normal protein. This amount is not enough to produce the same phenotype as the homozygous RR, which can produce twice this protein.

In this example, a reasonable explanation is that 50% of the functional protein can not achieve the same level of pigment synthesis as 100% of the protein.

The peas of Mendel's experiment ( Pisum sativum )

Mendel studied the characteristic of the pea seed form and visually concluded that the RR and Rr genotypes produced round seeds, while the rr genotype produced wrinkled seeds.

However, the closer it is observed, it becomes more evident that the heterozygote is not so similar to the wild-type homozygote. The peculiar morphology of the wrinkled seed is caused by a large decrease in the amount of starch deposition in the seed due to a defective r allele.

More recently, other scientists have dissected round and wrinkled seeds and examined their contents under the microscope . They found that round seeds of heterozygotes actually contain an intermediate number of starch grains compared to the seeds of homozygotes.

What happens is that, within the seed, an intermediate amount of the functional protein is not enough to produce as many starch grains as in the homozygous carrier.

In this way, the opinion about whether a trait is dominant or incomplete dominant may depend on how closely the trait is examined in the individual.

The enzyme hexosaminidase A (Hex-A)

Some inherited diseases are caused by enzymatic deficiencies; that is, by the lack or insufficiency of some protein necessary for the normal metabolism of cells. For example, Tay-Sachs disease is caused by a deficiency of the Hex-A protein.

Individuals who are heterozygous for this disease-that is, those who have a wild-type allele that produces the functional enzyme and a mutant allele that does not produce the enzyme-are individuals as healthy as homozygous wild individuals.

However, if the phenotype is based on the level of the enzyme, then the heterozygote has an intermediate level of enzyme between the homozygous dominant (full enzyme level) and homozygous recessive (no enzyme). In cases like this, half the normal amount of enzyme is sufficient for health.

Familial hypercholesterolemia

Familial hypercholesterolemia is an example of incomplete dominance that can be observed in carriers, both in the molecular and the body. A person with two alleles that cause the disease lacks receptors in liver cells.

These receptors are responsible for taking cholesterol, in the form of low density lipoprotein (LDL), from the bloodstream. Therefore, people who do not possess these receptors accumulate LDL molecules.

A person with a single mutant allele (causing disease) has half the normal number of receptors. Someone with two wild type alleles (do not cause the disease) has the normal amount of receptors.

The phenotypes are parallel to the number of receptors: individuals with two mutant alleles die in childhood from heart attacks, those with a mutant allele can suffer heart attacks in early adulthood, and those with two wild-type alleles do not develop this form hereditary of heart disease.

References

1. Brooker, R. (2012). Concepts of Genetics (1st ed.). The McGraw-Hill Companies, Inc.
2. Chiras, D. (2018). Human Biology (9 ^th ). Jones & Bartlett Learning.
3. Cummins, M. (2008). Human Heredity: Principles and Issues (8 ^th ). Cengage Learning
4. Dashek, W. & Harrison, M. (2006). Plant Cell Biology (1 ^st ). CRC Press.
5. Griffiths, A., Wessler, S., Carroll, S. & Doebley, J. (2015). Introduction to Genetic Analysis (11th ed.). W.H. Freeman
6. Lewis, R. (2015). Human Genetics: Concepts and Applications (11th ed.). McGraw-Hill Education.
7. Snustad, D. & Simmons, M. (2011). Principles of Genetics (6th ed.). John Wiley and Sons.
8. Windelspecht, M. (2007). Genetics 101 (1st ed.). Greenwood