An epistatic genetic basis for fluctuating asymmetry of tooth size and shape in mice

Abstract

Although there typically is little additive genetic variation for fluctuating asymmetry (FA), or variation in nondirectional differences between left and right sides of bilateral characters, several investigators have hypothesized that FA may have an epistatic genetic basis. We tested this hypothesis by conducting a whole genome scan of FA of size and shape of the mandibular molars in house mice from an F 2 intercross population generated from crossing the Large (LG/J) and Small (SM/J) inbred strains. Although no individual genes (QTLs ¼ quantitative trait loci) on any of the 19 autosomes significantly affected FA for centroid size, and only two affected shape FA, a number of pairwise combinations of QTLs exhibited significant epistasis for FA in both molar size and shape. The QTLs involved in these interactions differed for FA in molar size versus FA in molar shape, but their epistatic contributions to the total variance was nearly the same (about 20%) for FA in both molar characters. It was noted that the genetic architecture of FA in the molar characters, consisting of little or no additive genetic variance but an abundance of epistatic genetic variance, is consistent with that of other typical fitness components such as litter size. Heredity (2005) 94, 316-325.

The Genetic Architecture of Fluctuating Asymmetry of Mandible Size and Shape in a Population of Mice: Another Look

“…Given that 74.3% of these epistatic interactions are expected to be true positives, this suggests that epistasis accounts for about 20.6% of the FASIZE variation. Although we cannot know the actual impact of epistasis on FASIZE in the F3 mice, it does appear that it is comparable to that previously found for FA of mandible size [20] or molar size [47] in the F2 mice.…”

“…Leamy et al [20] did not analyze FA of mandible shape in their previous study, but did find comparable levels of epistatic effects for both FA of size and FA of shape in molars in the same F2 mouse population. In that study, the level of measurement error for molar shape (22%) was quite high, but was only 2.5 times that (8.9%) for molar size [47].…”

“…Thus the impact of epistasis on FASHAPE is considerably higher than that for single-locus effects. Leamy et al [47] also found that epistatic effects contributed far more than single-locus effects to the variation in FA of molar shape in the F2 mice. Clearly there is very little additive genetic variation for FA in these mandible traits, and this continues to be the general expectation for FA in a number of other traits as well [10,47].…”

“…Leamy et al [47] also found that epistatic effects contributed far more than single-locus effects to the variation in FA of molar shape in the F2 mice. Clearly there is very little additive genetic variation for FA in these mandible traits, and this continues to be the general expectation for FA in a number of other traits as well [10,47]. On the other hand, nonlinear developmental models for the origin of developmental instability suggest that nonadditive genetic effects, including epistasis, are expected to be an important part of the genetic architecture of FA [6].…”

“…In previous studies with the F2 generation mice, several epistatic combinations affecting FA in both mandible size [20] and tooth size [47] (LOD = 4.27). On the other hand, testing for epistasis in the F2 mice was done using a physiological epistasis model [48] which was criticized by Zeng et al [49].…”