Changes in Genetic Variance Induced by Random Genetic Drift

We noted in Chapter 2 that when operating as the sole evolutionary force, random genetic drift leads inevitably to the loss of alleles within populations as well as to the fixation of alternative alleles in different populations. These conclusions extend logically to quantitative characters. Following a reduction in population size, for example, we expect the genetic variance within populations to decline and the mean phenotypes of isolated populations to diverge. There are some interesting surprises, however, particularly when the mode of gene action has a nonadditive component. In the latter case, the genetic variance for a trait is not a simple function of the underlying heterozygosity (LW Chapter 4), so we cannot expect the temporal dynamics of genetic variance to strictly reflect patterns of heterozygosity. Indeed, as will be shown below, under certain conditions, the genetic variance for a quantitative trait is expected to transiently increase during the early phase of a population bottleneck. The goal of the following two chapters is to develop a null (neutral) hypothesis for quantitative-trait evolution, under the assumption that selection is a negligible evolutionary force. For the most part, we will continue to adhere to an ideal Wright-Fisher form of population structure, with random mating and discrete generations. In this vein, our conceptual approach will be to consider a series of replicate populations , all isolated at the same time from a large base population, generally assumed to be in Hardy-Weinberg and gametic-phase equilibrium, and all subsequently kept indefinitely at an identical population size. The current chapter focuses on the the expected dynamics of the genetic variance within populations, whereas Chapter 6 focuses on interpopulational divergence. In both chapters, we will initially assume that the dynamics of evolutionary change are due entirely to genetic properties of the base population, which is essentially the case with short-term population bottlenecks. Then, the role of mutation