Prevalent positive epistasis
in Escherichia coli and Saccharomyces cerevisiae metabolic networks.
Understanding biological epistasis
is one important motivation for studying statistical epistasis
is a population property, and is a function of both the allele frequencies and the biological interactions among genes (Carter et al.
and the effect of founder events on the additive genetic variance.
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
Single QTL effects, epistasis
, and pleiotropy account for two-thirds of the phenotypic F(2) variance of growth and obesity in DU6ixDBA/2 mice.