Classical Mendelian genetics established that traits are passed down via discrete units, where one allele, or gene variant, can completely mask the effect of another. However, not all gene pairs operate under this simple dominant-recessive relationship. Alternative patterns of expression exist where the interaction between two alleles results in a third, distinct phenotype. Understanding these variations in genetic expression is important for grasping the full spectrum of biological diversity.
The Fundamental Mechanism of Incomplete Dominance
Incomplete dominance describes a pattern of inheritance where the heterozygous genotype results in a physical trait that is intermediate between the two homozygous phenotypes. In this scenario, neither allele completely asserts its effect over the other, leading to a third phenotype that appears to be a physical blending of the two parental traits.
A classic illustration of this mechanism is found in the flower color of the snapdragon plant, Antirrhinum majus. When a plant homozygous for red flowers is crossed with a plant homozygous for white flowers, the offspring are all pink. The pink color is an entirely new phenotype, distinct from either parent color.
The molecular basis for this intermediate expression often relates to the dosage effect. One allele typically codes for a functional protein, such as an enzyme necessary for pigment production, while the other allele may be non-functional. A homozygous red-flowered plant possesses two functional alleles, producing a full dose of the red pigment enzyme. In the heterozygous pink-flowered plant, only one functional allele is present, which produces about half the amount of the pigment-producing enzyme compared to the homozygous red plant. This reduced quantity of enzyme is not enough to synthesize the full concentration of red pigment, creating the visually lighter, pink phenotype.
Distinguishing Incomplete Dominance from Codominance
Incomplete dominance and codominance are fundamentally different in how the alleles are expressed in the heterozygote. The key distinction lies in the appearance of the heterozygous individual. In incomplete dominance, the result is an intermediate, blended phenotype.
Codominance, conversely, involves the simultaneous and separate expression of both alleles in the heterozygote. Instead of blending to form a new trait, both parental traits are expressed fully and side-by-side. The presence of one allele does not dilute or modify the expression of the other.
A clear example of codominance in humans is the ABO blood group system, specifically the AB blood type. An individual with the A allele and the B allele expresses both A and B antigens fully on the surface of their red blood cells. The A antigen is not partially expressed, nor is the B antigen reduced; both are present in their entirety. If the inheritance of the A and B alleles followed incomplete dominance, the resulting blood type would be some third, blended type that was neither A nor B, which is not the case.
Human Traits Exhibiting Incomplete Dominance Patterns
Several human traits are cited to illustrate the pattern of incomplete dominance, despite many being governed by complex polygenic inheritance. Hair texture is a common physical trait that appears to follow this pattern. Individuals who are homozygous for the allele for curly hair typically have very tight curls, while those homozygous for the straight hair allele have straight hair. The heterozygous state, possessing one allele for curly and one for straight, often results in wavy hair. Wavy hair is visually intermediate between the two homozygous extremes because the protein structure is only partially modified by the single curly allele.
Incomplete dominance is also observed in Familial Hypercholesterolemia (FH), a condition characterized by high blood cholesterol levels. FH is caused by a defect in the gene responsible for producing low-density lipoprotein (LDL) receptors, which remove LDL cholesterol from the bloodstream.
A person with the homozygous wild-type genotype has a normal number of functional LDL receptors and healthy cholesterol levels. Individuals who are homozygous for the mutant FH allele produce almost no functional receptors, resulting in extremely severe, life-threatening cholesterol levels. The heterozygous individual, having one normal allele and one mutant allele, produces an intermediate number of functional LDL receptors. This reduced number of receptors results in elevated, though typically less severe, cholesterol levels compared to the homozygous mutant, illustrating incomplete dominance in a human health context.