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RSC Mobilizes Nucleosomes To Improve Accessibility of Repair Machinery to the Damaged Chromatin

机译：RSC动员核小体以改善修复机器对受损染色质的可及性

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Repair of DNA double-strand breaks (DSBs) protects cells and organisms, as well as their genome integrity. Since DSB repair occurs in the context of chromatin, chromatin must be modified to prevent it from inhibiting DSB repair. Evidence supports the role of histone modifications and ATP-dependent chromatin remodeling in repair and signaling of chromosome DSBs. The key questions are, then, what the nature of chromatin altered by DSBs is and how remodeling of chromatin facilitates DSB repair. Here we report a chromatin alteration caused by a single HO endonuclease-generated DSB at the Saccharomyces cerevisiae MAT locus. The break induces rapid nucleosome migration to form histone-free DNA of a few hundred base pairs immediately adjacent to the break. The DSB-induced nucleosome repositioning appears independent of end processing, since it still occurs when the 5′-to-3′ degradation of the DNA end is markedly reduced. The tetracycline-controlled depletion of Sth1, the ATPase of RSC, or deletion of RSC2 severely reduces chromatin remodeling and loading of Mre11 and Yku proteins at the DSB. Depletion of Sth1 also reduces phosphorylation of H2A, processing, and joining of DSBs. We propose that RSC-mediated chromatin remodeling at the DSB prepares chromatin to allow repair machinery to access the break and is vital for efficient DSB repair.
机译：DNA双链断裂（DSB）的修复可保护细胞和生物及其基因组完整性。由于DSB修复发生在染色质的背景下，必须修饰染色质以防止其抑制DSB修复。证据支持组蛋白修饰和ATP依赖的染色质重塑在染色体DSB的修复和信号传导中的作用。那么，关键问题是DSB改变了染色质的本质，以及染色质的重塑如何促进DSB修复。在这里，我们报告了由酿酒酵母MAT 位点的单个HO内切核酸酶生成的DSB引起的染色质改变。该断裂引起快速的核小体迁移，以形成紧邻断裂的数百个碱基对的无组蛋白的DNA。 DSB诱导的核小体重新定位似乎与末端处理无关，因为当DNA末端的5'至3'降解显着减少时，它仍然会发生。四环素控制的Sth1耗尽，RSC的ATPase或 RSC2 的缺失严重降低了染色质重塑以及DSB处Mre11和Yku蛋白的负载。 Sth1的耗尽还减少了H2A的磷酸化，加工和DSB的连接。我们建议，在DSB处RSC介导的染色质重塑可以制备染色质，以使维修机械能够进入断裂点，这对于有效的DSB维修至关重要。

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