BOTTLENECK EFFECT ON GENETIC VARIANCE - A THEORETICAL INVESTIGATION OF THE ROLE OF DOMINANCE

The phenomenon that the genetic variance of fitness components increas e following a bottleneck or inbreeding is supported by a growing numbe r of experiments and is explained theoretically by either dominance or epistasis. In this article, diffusion approximations under the infini te sites model are used to quantify the effect of dominance, using dat a on viability in Drosophila melanogaster. The model is based on mutat ion parameters from mutation accumulation experiments involving balanc er chromosomes (set I) or inbred lines (set II). In essence, set I ass umes many mutations of small effect, whereas set II assumes fewer muta tions of large effect. Compared to empirical estimates from large outb red populations, set I predicts reasonable genetic variances but too l ow mean viability. In contrast, set II predicts a reasonable mean viab ility but a low genetic variance. Both sets of parameters predict the changes in mean viability (depression), additive variance, between-lin e variance and heritability following bottlenecks generally compatible with empirical results, and these changes are mainly caused by lethal s and deleterious mutants of large effect. This article suggests that dominance is the main cause for increased genetic variances for fitnes s components and fitness-related traits after bottlenecks observed in various experiments.