Hybrid sterility is one of the reproductive isolation mechanisms leading to speciation. Prdm9, the only known vertebrate hybrid-sterility gene, causes failure of meiotic chromosome synapsis and infertility in male hybrids that are the offspring of two mouse subspecies. Within species, Prdm9 determines the sites of programmed DNA double-strand breaks (DSBs) and meiotic recombination hotspots. To investigate the relation between Prdm9-controlled meiotic arrest and asynapsis, we inserted random stretches of consubspecific homology on several autosomal pairs in sterile hybrids, and analyzed their ability to form synaptonemal complexes and to rescue male fertility. Twenty-seven or more megabases of consubspecific (belonging to the same subspecies) homology fully restored synapsis in a given autosomal pair, and we predicted that two or more DSBs within symmetric hotspots per chromosome are necessary for successful meiosis. We hypothesize that impaired recombination between evolutionarily diverged chromosomes could function as one of the mechanisms of hybrid sterility occurring in various sexually reproducing species.

中文翻译：

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调节 Prdm9 控制的减数分裂染色体突触超越了小鼠的杂交不育性

杂交不育是导致物种形成的生殖隔离机制之一。Prdm9 是唯一已知的脊椎动物杂种不育基因，可导致作为两个小鼠亚种后代的雄性杂种的减数分裂染色体突触失败和不育。在物种内，Prdm9 确定程序化 DNA 双链断裂 (DSB) 和减数分裂重组热点的位点。为了研究 Prdm9 控制的减数分裂停滞与不联会之间的关系，我们在不育杂种中的几个常染色体对上插入了随机的亚种同源序列，并分析了它们形成联会复合物和挽救雄性生育力的能力。在给定的常染色体对中，27 个或更多兆碱基的同亚种（属于同一亚种）同源性完全恢复了突触，我们预测每个染色体对称热点内的两个或多个 DSB 是成功减数分裂所必需的。我们假设进化分化的染色体之间受损的重组可能是各种有性繁殖物种中发生的杂交不育机制之一。