WHAT IS INCOMPLETE DOMINANCE? (WITH EXAMPLES) - BIOLOGY - 2025

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

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

Intermediate phenotype in the F1 generation caused by incomplete dominance

The effect of incomplete dominance becomes evident when heterozygous offspring of a cross between homozygous are observed.

In this case, the offspring 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 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 appearance of the offspring is the result of the partial influence of both alleles or genes. Incomplete dominance occurs in polygenic inheritance (many genes) of traits such as eye, flower, and skin color.

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 from Correns's experiment (

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

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

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

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

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

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

What happens at the molecular level 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 gene regulation, heterozygotes can produce only 50% of normal protein. This amount is not enough to produce the same phenotype as the homozygous RR, which can produce twice as much this protein.

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

The peas from Mendel's experiment (

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

However, the closer you look, the more evident it becomes that the heterozygote is not as similar to the wild-type homozygous. 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, wrinkled seeds and examined their contents under the microscope. They found that the 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 sufficient to produce as many grains of starch as in the homozygous carrier.

Thus, the opinion about whether a trait is dominant or incompletely 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 enzyme deficiencies; that is, due to the lack or insufficiency of some protein necessary for normal cell metabolism. 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 with a wild-type allele that produces the functional enzyme and a mutant allele that does not produce the enzyme — are just as healthy individuals as homozygous wild-type individuals.

However, if the phenotype is based on the level of the enzyme, then the heterozygous has an intermediate level of enzyme between 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 at the molecular and bodily level. A person with two alleles that cause the disease lacks receptors on liver cells.

These receptors are responsible for taking cholesterol, in the form of low-density lipoprotein (LDL), from the bloodstream. Therefore, people without these receptors accumulate LDL molecules.

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

The phenotypes parallel the number of receptors: individuals with two mutant alleles die in infancy from heart attacks, those with one mutant allele may have heart attacks in early adulthood, and those with two wild-type alleles do not develop this form. hereditary heart disease.

References

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