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Accelerated Evolution of the Prdm9 Speciation Gene across Diverse Metazoan Taxa

机译：跨越多元化群分类群的PRDM9物种基因的加速演变

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The onset of prezygotic and postzygotic barriers to gene flow between populations is a hallmark of speciation. One of the earliest postzygotic isolating barriers to arise between incipient species is the sterility of the heterogametic sex in interspecies' hybrids. Four genes that underlie hybrid sterility have been identified in animals: Odysseus, JYalpha, and Overdrive in Drosophila and Prdm9 (Meisetz) in mice. Mouse Prdm9 encodes a protein with a KRAB motif, a histone methyltransferase domain and several zinc fingers. The difference of a single zinc finger distinguishes Prdm9 alleles that cause hybrid sterility from those that do not. We find that concerted evolution and positive selection have rapidly altered the number and sequence of Prdm9 zinc fingers across 13 rodent genomes. The patterns of positive selection in Prdm9 zinc fingers imply that rapid evolution has acted on the interface between the Prdm9 protein and the DNA sequences to which it binds. Similar patterns are apparent for Prdm9 zinc fingers for diverse metazoans, including primates. Indeed, allelic variation at the DNA–binding positions of human PRDM9 zinc fingers show significant association with decreased risk of infertility. Prdm9 thus plays a role in determining male sterility both between species (mouse) and within species (human). The recurrent episodes of positive selection acting on Prdm9 suggest that the DNA sequences to which it binds must also be evolving rapidly. Our findings do not identify the nature of the underlying DNA sequences, but argue against the proposed role of Prdm9 as an essential transcription factor in mouse meiosis. We propose a hypothetical model in which incompatibilities between Prdm9-binding specificity and satellite DNAs provide the molecular basis for Prdm9-mediated hybrid sterility. We suggest that Prdm9 should be investigated as a candidate gene in other instances of hybrid sterility in metazoans.
机译：Prezygotic和ProTzycotic屏障对种群之间的基因流动的发作是物种的标志。在初期物种之间出现的最早的Pertzygotic隔离障碍之一是杂种杂种中的杂种性别的无菌性。在动物中鉴定出杂种无菌的四个基因：奥德赛斯，朱尔斑和过载于果鼠的果蝇和PRDM9（Meisetz）。小鼠PRDM9用Krab基序，组蛋白甲基转移酶结构域和几种锌指编码蛋白质。单一锌指的差异区分PRDM9等位基因导致杂交无菌性来自那些没有的杂交性。我们发现协同的演化和肯定选择迅速改变了13个啮齿动物基因组的PRDM9锌手指的数量和序列。 PRDM9锌指的阳性选择的模式意味着快速进化已经作用于PRDM9蛋白与其结合的DNA序列之间的界面。对于不同的聚美唑诺亚，类似的图案对于PRDM9锌指的是显而易见的，包括灵长类动物。实际上，人PRDM9锌指的DNA结合位置的等位基因变异表现出与不孕症的风险降低的显着关联。因此，PRDM9在确定物种（小鼠）和物种（人）内的雄性不育中起作用。作用于PRDM9的阳性选择的复发事件表明它结合的DNA序列也必须快速发展。我们的研究结果不识别潜在的DNA序列的性质，但争论PRDM9作为小鼠减数分裂中必不可少的转录因子的拟议作用。我们提出了一种假设模型，其中PRDM9结合特异性和卫星DNA之间的不兼容性为PRDM9介导的杂化无菌提供了分子基础。我们建议应在美唑烷中的其他杂交无菌性实例中调查PRDM9作为候选基因。

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