epistasis
Huang W, Richards S, Carbone MA, Zhu D, Anholt RRH, Ayroles JF, Duncan L, Jordan KW, Lawrence F, Magwire MM, Warner CB, Blankenburg K, Han Y, Javaid M, Jayaseelan J, Jhangiani SN, Muzny D, Ongeri F, Perales L, Wu Y-Q, Zhang Y, Zou X, Stone EA, Gibbs RA & Mackay TFC 2012 Epistasis dominates the genetic architecture of Drosophila quantitative traits. PNAS 109:15553-15559.
- the crux of the controversy stems from the disparate goals of assessing the extent to which interactions affect mean genotypic values vs. estimating the fraction of total genetic variance caused by epistatic interactions in outbred populations
- nonadditive gene action does not translate to nonadditive genetic variance
- pure dominance results in mostly additive variance across the entire range of allele frequencies
- pure epistasis gives largely additive genetic variance when allele frequencies are low, and most frequencies are low
- in practice, all estimates of additive genetic variance (and hence, narrow sense heritability) from resemblance among relatives include fractions of the interaction variance
- purely epistatic models can result in covariance between relatives (5) and a substantial amount of apparent additive variance
- epistatic gene action causes largely additive genetic variance in natural populations in which the allele frequency spectrum is U-shaped
- hence, it is thought to be of little importance in predicting the response to directional selection
- it remains important to distinguish between genetic variation that is caused by epistasis and the fraction of genetic variation that can be statistically explained by an additive model
