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首页> 外文期刊>Molecular and Cellular Biology >Rhp51-Dependent Recombination Intermediates That Do Not Generate Checkpoint Signal Are Accumulated in Schizosaccharomyces pombe rad60 and smc5/6 Mutants after Release from Replication Arrest
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Rhp51-Dependent Recombination Intermediates That Do Not Generate Checkpoint Signal Are Accumulated in Schizosaccharomyces pombe rad60 and smc5/6 Mutants after Release from Replication Arrest

机译：从复制逮捕释放后，裂殖酵母pombe rad60和smc5 / 6突变体中积累了不生成检查点信号的依赖Rhp51的重组中间体。

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The Schizosaccharomyces pombe rad60 gene is essential for cell growth and is involved in repairing DNA double-strand breaks. Rad60 physically interacts with and is functionally related to the structural maintenance of chromosomes 5 and 6 (SMC5/6) protein complex. In this study, we investigated the role of Rad60 in the recovery from the arrest of DNA replication induced by hydroxyurea (HU). rad60-1 mutant cells arrested mitosis normally when treated with HU. Significantly, Rad60 function is not required during HU arrest but is required on release. However, the mutant cells underwent aberrant mitosis accompanied by irregular segregation of chromosomes, and DNA replication was not completed, as revealed by pulsed-field gel electrophoresis. The deletion of rhp51 suppressed the aberrant mitosis of rad60-1 cells and caused mitotic arrest. These results suggest that Rhp51 and Rad60 are required for the restoration of a stalled or collapsed replication fork after release from the arrest of DNA replication by HU. The rad60-1 mutant was proficient in Rhp51 focus formation after release from the HU-induced arrest of DNA replication or DNA-damaging treatment. Furthermore, the lethality of a rad60-1 rqh1Δ double mutant was suppressed by the deletion of rhp51 or rhp57. These results suggest that Rad60 is required for recombination repair at a step downstream of Rhp51. We propose that Rhp51-dependent DNA structures that cannot activate the mitotic checkpoints accumulate in rad60-1 cells.
机译：粟酒裂殖酵母rad60 基因对于细胞生长至关重要，并参与修复DNA双链断裂。 Rad60与5号和6号染色体（SMC5 / 6）蛋白复合物的结构维护发生物理相互作用，并在功能上与之相关。在这项研究中，我们调查了Rad60在阻止羟基脲（HU）诱导的DNA复制中的恢复中的作用。经HU处理后， rad60 - 1 突变细胞可正常阻止有丝分裂。重要的是，HU停止期间不需要Rad60功能，但释放时则需要Rad60功能。然而，突变细胞经历了异常的有丝分裂，伴随着染色体的不规则分离，并且如脉冲场凝胶电泳所揭示的，DNA复制没有完成。 rhp51 的缺失抑制了 rad60 - 1 细胞的异常有丝分裂，并导致有丝分裂停滞。这些结果表明Rhp51和Rad60是从HU终止DNA复制释放后恢复停滞或折叠的复制叉所必需的。 rad60 - 1 突变体在从HU诱导的DNA复制抑制或DNA损伤处理中释放后，能够熟练地形成Rhp51焦点。此外， rad60 - 1rqh1Δ双重突变体的致死性被 rhp51 或 rhp57 的缺失所抑制。这些结果表明Rad60是Rhp51下游的重组修复所必需的。我们建议不能激活有丝分裂检查点的依赖Rhp51的DNA结构积累在 rad60 - 1 细胞中。

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