The genetic architecture of complex traits: significant differences can involve noncoding DNA and can be epistatic

Clark et al., in "A distant upstream enhancer at the maize domestication gene tb1 has pleiotropic effects on plant and inflorescent architecture," describe a significant QTL residing in noncoding (and largely repetitive) DNA far upstream of the affected gene (PubMed, Nature Genetics). I am reminded of the graduate genetics course given by Michael Freeling that I sat in on while a postdoc at Berkeley (in 1984, while studying the effects of transposable element insertions on gene expression in Drosophila in Gerry Rubin's lab). He emphasized epigenetic phenomenon and truly expected that novel molecular mechanisms (such as transposon instability) would reveal "a molecular clock that really ticks." From his web page it looks like he's continuing on the same tack today.

A paper in the previous month's issue of Nature Genetics (Carlborg et al., "Epistasis and the release of genetic variation during long-term selection," PubMed, Nature Genetics) reported a genetic network of four interacting loci affecting chicken growth ("Growth4, Growth6 and Growth12 had a significantly larger effect on growth in homozygous Growth9 individuals than [others]"). This kind of genetic interaction is precisely what any developmental geneticist would expect, yet breeders and population geneticists often cling to simple linear models. This paper will certainly help, not least of all because it involves a method for the detection of epistatic QTLs.