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The suppression of the effect of one gene by another.
A checking or stoppage of a hemorrhage or other discharge.
A scum or film of substance floating on the surface of urine.



the interaction of two nonallelic genes (that is, genes that are at different loci) whereby one of them, called the epistatic gene, suppresses the effect of the other one, called the hypostatic gene. Phenotypically, epistasis is manifested as a deviation from the segregation that would be expected in digenetic inheritance; in this case, however, there is no violation of Mendel’s laws, inasmuch as the alleles of the interacting genes are distributed in complete conformity to the law of independent assortment, or combination.

References in periodicals archive ?
Prevalent positive epistasis in Escherichia coli and Saccharomyces cerevisiae metabolic networks.
Understanding biological epistasis is one important motivation for studying statistical epistasis.
Statistical epistasis is a population property, and is a function of both the allele frequencies and the biological interactions among genes (Carter et al.
In fact, this is the first case of epistasis described in the alcohol consumption/alcohol dependence literature.
Classical quantitative genetic studies of crossbreds produced by crossing inbred lines have uncovered remarkable heterosis in growth and its physiological components at larval, juvenile and adult stages and has implicated epistasis as a significant cause of this heterosis (Hedgecock et al.
Various concepts of gene interaction or epistasis have been used in quantitative genetics, and its definition was recently extended even to the interaction between different genes each from a different individual (Wolf, 2000).
The significance of marker epistasis was indicated by the probability associated with the F value for the interaction of each pair of markers in the ANOVAs.
2002) extended the method of Dekkers and van Arendonk (1998) to selection programs with different selection strategies for males and females, maximizing a weighted combination of short and longer term responses, and to multiple identified QTL, allowing for non-additive effects at the QTL, including dominance, epistasis and gametic imprinting.
Finally, we estimated the genetic correlations among the variables as standard product-moment correlations among the family means for all pairs of traits (Falconer & Mackay 1996) For these estimates, we again used the block-adjusted data, and reduced these data to the means of 2 different types of families: (1) the six paternal half-sib families, which provides an estimate of the purely additive or strict sense genetic correlation and (2) the 26 full-sib family means, which, because of the inclusion of the nonadditive influences of dominance and epistasis, estimates the broad-sense genetic correlation.
Three hypotheses exist for explaining heterosis: dominance (Davenport, 1908), over-dominance (Shull, 1908) and epistasis (Wright, 1951).
Single QTL effects, epistasis, and pleiotropy account for two-thirds of the phenotypic F(2) variance of growth and obesity in DU6ixDBA/2 mice.