Epistatic

Epistatic interactions occur when the effect of an allele at one gene depends on the genotype at another gene. In effect, one gene can mask, enhance, or modify the phenotypic outcome produced by another gene. The concept arose from classical genetics; Bateson and Punnett introduced the term to describe deviations from simple Mendelian ratios in dihybrid crosses, emphasizing that genes do not act in isolation but within networks.

Epistasis can take several forms. In masking or dominant epistasis, the action of one gene overrides the effect of another gene's alleles. Recessive epistasis occurs when a recessive genotype at one locus masks expression at a second locus. More complex patterns include duplicate gene action, where two genes can compensate for each other to produce a trait, and complementary gene action, where both genes are required for a phenotype to appear. Epistasis can alter expected dihybrid ratios, producing non-Mendelian distributions of phenotypes.

Examples illustrate these interactions. Labrador retriever coat color is a classic case: the E locus determines pigment deposition, and when the genotype ee occurs, pigment is not deposited, yielding yellow regardless of the B locus. The Bombay phenotype in humans is another well-known example, where a separate gene masks the expression of ABO antigens. In plants and other animals, epistasis shapes traits such as flower color, fruit color, and metabolic products by coordinating steps in biochemical pathways.

Significance lies in its influence on inheritance patterns, genetic mapping, and breeding. Epistasis is also relevant to understanding complex diseases, where multiple genes interact to affect risk and phenotype.