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AN EPISTATIC GENETIC BASIS FOR FLUCTUATING ASYMMETRY OF MANDIBLE SIZE IN MICE
Author(s) -
Leamy Larry J.,
Routman Eric J.,
Cheverud James M.
Publication year - 2002
Publication title -
evolution
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.84
H-Index - 199
eISSN - 1558-5646
pISSN - 0014-3820
DOI - 10.1111/j.0014-3820.2002.tb01373.x
Subject(s) - epistasis , biology , genetic variation , population , effective population size , genetics , evolutionary biology , genetic architecture , quantitative trait locus , statistics , gene , mathematics , demography , sociology
The genetic basis of fluctuating asymmetry (FA), or nondirectional variation in the subtle differences between left and right sides of bilateral characters, continues to be of considerable theoretical interest. FA generally has been thought to arise from random noise during development and therefore to have a largely or entirely environmental origin. Whereas additive genetic variation for FA generally has been small and often insignificant, a number of investigators have hypothesized that interactions between loci, or epistasis, significantly influence FA. We tested this hypothesis by conducting a whole‐genome scan to detect any epistasis in FA of centroid size in the mandibles of more than 400 mice from an F 2 intercross population formed from crossing the Large (LG/J) and Small (SM/J) inbred strains. Genotypic deviations were imputed at each site 2 cM apart on all 19 autosomes, and these and centroid size asymmetry values were used in canonical correlation analyses for each of the 171 possible pairs of 19 autosomes to identify the most probable sites for epistasis. Epistasis for centroid size asymmetry was abundant, occurring far more often than was expected by chance alone (there were 30 separate instances of epistasis at the 0.001 significance level, when only two were expected by chance alone). The contributions of epistasis from 30 pairwise combinations of loci tended to suppress the additive and dominance genetic variance, but greatly increased the epistatic genetic variance for FA in centroid size given the intermediate allele frequencies of an F 2 intercross population.