A non-additive interaction between genes in which the phenotypic effect of an allele at one locus depends on the alleles present at one or more other loci.

Principle

Phenotypes arise from networks of interacting loci; allelic effects can be masked, enhanced, or altered by variants at interacting loci, producing departures from simple additive genetic models.

Demonstration

In a two-locus system, an allele that would produce pigment only does so when a second locus carries a permissive allele; when the second locus has a nonpermissive allele, the pigment phenotype is suppressed.

Misapplication

Labeling observed nonlinearity as epistasis without ruling out dominance at the same locus, genotype–environment interaction, or inadequately modeled population structure.

Consequence

Epistasis alters expected genotype–phenotype mappings, affects response to selection, complicates mapping of causal variants, and can generate conditional genetic effects observable only in certain backgrounds.

Reversal

A strictly additive genetic architecture where each locus contributes independently to phenotype and combined effects equal the sum of individual effects.

Boundary

Refers to interactions among genetic loci (including intra-locus interactions labeled dominance vs inter-locus epistasis); it does not by itself denote environmental modulation (G×E), though both can coexist.

Semantic Tension

Overlaps conceptually with dominance (interaction within a locus) and with statistical interaction terms in models; tension arises in distinguishing mechanistic epistasis from statistical epistatic signals caused by confounding.

Synthesis

Epistasis is the property of genetic systems where the effect of an allele depends on genetic context: interactions among loci produce non-additive phenotypic outcomes that must be identified by experimental designs separating locus-specific and population-level confounders.