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首页> 外文期刊>Molecular and Cellular Biology >Mus81-Eme1-Dependent and -Independent Crossovers Form in Mitotic Cells during Double-Strand Break Repair in Schizosaccharomyces pombe
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Mus81-Eme1-Dependent and -Independent Crossovers Form in Mitotic Cells during Double-Strand Break Repair in Schizosaccharomyces pombe

机译：粟酒裂殖酵母双链断裂修复过程中有丝分裂细胞中Mus81-Eme1依赖和独立的交叉形式。

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During meiosis, double-strand breaks (DSBs) lead to crossovers, thought to arise from the resolution of double Holliday junctions (HJs) by an HJ resolvase. In Schizosaccharomyces pombe, meiotic crossovers are produced primarily through a mechanism requiring the Mus81-Eme1 endonuclease complex. Less is known about the processes that produces crossovers during the repair of DSBs in mitotic cells. We employed an inducible DSB system to determine the role of Rqh1-Top3 and Mus81-Eme1 in mitotic DSB repair and crossover formation in S. pombe. In agreement with the meiotic data, crossovers are suppressed in cells lacking Mus81-Eme1. And relative to the wild type, rqh1Δ cells show a fourfold increase in crossover frequency. This suppression of crossover formation by Rqh1 is dependent on its helicase activity. We found that the synthetic lethality of cells lacking both Rqh1 and Eme1 is suppressed by loss of swi5+, which allowed us to show that the excess crossovers formed in an rqh1Δ background are independent of Mus81-Eme1. This result suggests that a second process for crossover formation exists in S. pombe and is consistent with our finding that deletion of swi5+ restored meiotic crossovers in eme1Δ cells. Evidence suggesting that Rqh1 also acts downstream of Swi5 in crossover formation was uncovered in these studies. Our results suggest that during Rhp51-dependent repair of DSBs, Rqh1-Top3 suppresses crossovers in the Rhp57-dependent pathway while Mus81-Eme1 and possibly Rqh1 promote crossovers in the Swi5-dependent pathway.
机译：在减数分裂期间，双链断裂（DSB）导致交叉，这被认为是由HJ分解酶对双霍利迪结（HJs）的分辨引起的。在裂殖酵母中，减数分裂的产生主要是通过需要Mus81-Eme1内切核酸酶复合物的机制产生的。关于在有丝分裂细胞中DSB修复过程中产生交换的过程所知甚少。我们采用了诱导型DSB系统来确定Rqh1-Top3和Mus81-Eme1在 S中的有丝分裂DSB修复和交叉形成中的作用。蓬贝。与减数分裂数据一致，缺少Mus81-Eme1的细胞中的交叉被抑制。相对于野生型， rqh1 Δ细胞的交叉频率增加了四倍。 Rqh1对交叉形成的抑制取决于其解旋酶活性。我们发现缺少 swi5 + 可以抑制同时缺少Rqh1和Eme1的细胞的合成杀伤力，这使我们证明了 rqh1 Δ背景独立于Mus81-Eme1。该结果表明在 S中存在形成交叉的第二过程。 pombe ，并且与我们的发现一致：删除 swi5 + 可以恢复 eme1 Δ细胞的减数分裂交叉。在这些研究中没有发现证据表明Rqh1在交叉形成中也作用于Swi5的下游。我们的结果表明，在DSB依赖Rhp51的修复过程中，Rqh1-Top3抑制Rhp57依赖性途径中的交叉，而Mus81-Eme1和可能的Rqh1促进Swi5依赖性途径中的交叉。

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