Brookfield J F, Badge R M
Department of Genetics, University of Nottingham, Queens Medical Centre, UK.
Genetica. 1997;100(1-3):281-94.
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.
转座元件拷贝数的控制具有相当大的理论和实证研究价值。在简单模型下，拷贝数可能会无限制增加。能够阻止这种增加的机制包括：选择效应随拷贝数增加而增强的机制；转座率随拷贝数降低的机制；以及转座元件家族中功能异质性的后果阻止拷贝数无限制增加的机制。有限的种群规模可能会以多种方式削弱自然选择作用于转座元件拷贝数的能力，这在实验室种群中可能尤为重要。首先，宿主种群规模较小会偶尔出现拷贝数个体间差异减小的时期，随之自然选择的能力也会减弱，即便预期差异为泊松分布。其次，小种群规模会产生高频转座元件位点，系统性地降低拷贝数的差异。当转座元件的杂合性导致其产生选择性损伤时，比如异位交换限制拷贝数时，其后果会尤为严重。
