epistasis

Hurst LD 2000 Epistasis and the evolutionary process. Heredity 85:625-626.

  • review of: Wolf JB, Brodie ED III & Wade MJ, eds. 2000 Epistasis and the evolutionary process. Oxford UP. ISBN:9780195128060
  • Brodie suggests that Fisher, when analysing adaptive evolution, considered a model in which mutants at a locus went through to fixation so fast that no interacting allelic variants at other loci were around to disrupt the process
  • this defends the use of single locus models but does not explain why the assumption was made
  • most consider that Fisher was imagining a model in which, because of recombination, the background that any given allele would sit in was constantly churning so the average effect was all that we needed to consider
  • the average might well approximate to multiplicativity if ε is greater then zero, as often as it is less than zero
  • Phillips, Otto and Whitlock make, I think, a most telling point
  • even if Fisher was right that on average ε is about zero, the little studied variance in ε still matters
  • is epistasis everywhere?
  • many studies say not
  • but here Templeton provides possibly the most incisive of the chapters in arguing that standard modes of analysis have such a baggage of Fisherian assumptions
  • it is actually biased against finding epistasis
  • it simply being what is left over when all other sources of variance are removed
  • Wright's view, antithetical to that of Fisher, was that epistasis was important because after population sub-division, the epistatic effects would allow different phenotypes in different sub-populations
  • without needing to evoke selection and local adaptation
  • the finding that additive variation increases after bottlenecking, reviewed separately by Meffert and Goodnight, is strong support for Wright's position
  • (or at least some version of it)
  • this result is quite the opposite of what the simple Fisherian models would predict
  • the Wrightian ancestry of many involved in epistasis research also goes a long way to explaining why all but one of the 24 authors is at a North American institute
  • (and the other is an American abroad)
  • as Brodie makes clear, effects that are additive for phenotype can be non-additive for fitness
  • and vice versa
  • the introductory chapter by Brodie attempts to do the same graphically but leaves more problems than answers
  • without exception the chapters are well considered and reach guarded conclusions
  • in this context it was rather fun to see Wade cite a particularly strong and unguarded assertion from Brian Charlesworth
  • in a letter to Norm Johnson he posits that 'this relentless and futile search for intraspecific epistasis needs to be abandoned!'
  • the book convinced me that Charlesworth is wrong on this one