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EPISTASIS AND THE EVOLUTION OF ADDITIVE GENETIC VARIANCE IN POPULATIONS THAT PASS THROUGH A BOTTLENECK
Author(s) -
Cheverud James M.,
Vaughn Ty T.,
Pletscher L. Susan,
KingEllison Kelly,
Bailiff Jeff,
Adams Emily,
Erickson Christopher,
Bonislawski Adam
Publication year - 1999
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.1558-5646.1999.tb04516.x
Subject(s) - biology , epistasis , bottleneck , evolutionary biology , variance (accounting) , population bottleneck , genetics , allele , gene , computer science , microsatellite , embedded system , accounting , business
Traditional models of genetic drift predict a linear decrease in additive genetic variance for populations passing through a bottleneck. This perceived lack of heritable variance limits the scope of founder‐effect models of speciation. We produced 55 replicate bottleneck populations maintained at two male‐female pairs through four generations of inbreeding (average F = 0.39). These populations were formed from an F 2 intercross of the LG/J and SM/J inbred mouse strains. Two contemporaneous control strains maintained with more than 60 mating pairs per generation were formed from this same source population. The average level of within‐strain additive genetic variance for adult body weight was compared between the control and experimental lines. Additive genetic variance for adult body weight within experimental bottleneck strains was significantly higher than expected under an additive genetic model This enhancement of additive genetic variance under inbreeding is likely to be due to epistasis, which retards or reverses the loss of additive genetic variance under inbreeding for adult body weight in this population. Therefore, founder‐effect speciation processes may not be constrained by a loss of heritable variance due to population bottlenecks.