Population genetics models of transposable elements

Abstract

The control of transposable element copy number is of considerable theoretical and empirical interest. Under simple models, copy numbers may increase without limit. Mechanisms that can prevent such an increase include those in which the effect of selection increases with copy number, those in which the rate of transposition decreases with copy number, and those where unlimited increase in copy number is prevented by the consequences of functional heterogeneity in the transposable element family. Finite population sizes may attenuate the power of natural selection to act on transposable element copy number in a number of ways that may be of particular importance in laboratory populations. First, a small host population size will create occasional periods in which the variance between individuals in copy number is diminished, and with it the power of natural selection, even when the expected variance is Poisson. Second, small population sizes will produce high-frequency transposable element sites, systematically reducing the variance in copy number. The consequences will be particularly profound when the selective damage of transposable elements follows from their heterozygosity, as when ectopic exchange limits copy number.