Quesneville H, Anxolabéhère D
Laboratoire de Dynamique du Génome et Evolution, Institut Jacques Monod, Paris, France.
Theor Popul Biol. 1998 Oct;54(2):175-93. doi: 10.1006/tpbi.1997.1353.
Work on how transposable elements are maintained and spread by virtue of their transposition processes have produced many theoretical studies of their evolutionary dynamics. But recent studies, which have experimentally identified some of these mechanisms, have not been taken into account. We present an integrated model of P transposable element regulation. It includes, at an individual level, the various mechanisms of regulation and the transposition events, that have been experimentally identified, recording specifically the chromosomal localisations of the inserted copies. It attempts to define the minimum conditions for explaining the regulation and spread of the P transposable element in Drosophila melanogaster natural populations. One test of this model is that it must explain the different population states found in the wild. A program that simulates the changes in Drosophila populations during the invasion of P elements was developed; the simulated populations were then compared to natural population data at the molecular and genetic levels. The model was validated by testing the dynamics of P element invasion in populations. It could explain the different natural population states with a recurrent invasion process. The simulations show that migration reduces the total number of copies, increases the number of defective copies, decreases P-activity and increases P-susceptibility, shifting equilibrium states from P to M'. They also show that the copies determining P-cytotype regulation spread faster by selection when located on the X chromosome. This result could account for the unexplained accumulation of P copies on the X chromosomes of some natural populations. Moreover the simulations predict a novel equilibrium state, called P', not yet characterized in natural populations but that can be found in natural population data.
关于转座元件如何凭借其转座过程得以维持和传播的研究,已经产生了许多关于其进化动力学的理论研究。但最近那些通过实验确定了其中一些机制的研究却未被考虑在内。我们提出了一个P转座元件调控的综合模型。在个体层面,它涵盖了已通过实验确定的各种调控机制和转座事件,特别记录了插入拷贝的染色体定位。它试图确定解释P转座元件在黑腹果蝇自然种群中调控和传播的最小条件。对该模型的一个检验是,它必须解释在野外发现的不同种群状态。开发了一个模拟P元件入侵期间果蝇种群变化的程序;然后将模拟种群与分子和遗传水平的自然种群数据进行比较。通过测试种群中P元件入侵的动态过程对该模型进行了验证。它可以通过反复入侵过程来解释不同的自然种群状态。模拟结果表明,迁移减少了拷贝总数,增加了缺陷拷贝的数量,降低了P活性并增加了P易感性,使平衡状态从P型转变为M'型。模拟还表明,决定P细胞型调控的拷贝位于X染色体上时,通过选择传播得更快。这一结果可以解释一些自然种群X染色体上P拷贝无法解释的积累现象。此外,模拟预测了一种新的平衡状态,称为P'型,在自然种群中尚未得到表征,但可以在自然种群数据中找到。