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首页> 外文期刊>Molecular cell >Chromosome-wide Rad51 spreading and SUMO-H2A.Z-dependent chromosome fixation in response to a persistent DNA double-strand break.
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Chromosome-wide Rad51 spreading and SUMO-H2A.Z-dependent chromosome fixation in response to a persistent DNA double-strand break.

机译：遍及整个染色体的Rad51扩散和SUMO-H2A.Z依赖的染色体固定，响应持续的DNA双链断裂。

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摘要

DNA double-strand breaks (DSBs) are acutely hazardous for cells, as they can cause genome instability. DSB repair involves the sequential recruitment of repair factors to the DSBs, followed by Rad51-mediated homology probing, DNA synthesis, and ligation. However, little is known about how cells react if no homology is found and DSBs persist. Here, by monitoring a single persistent DNA break, we show that, following DNA resection and RPA recruitment, Rad51 spreads chromosome-wide bidirectionally from the DSB but selectively only on the broken chromosome. Remarkably, the persistent DSB is later fixed to the nuclear periphery in a process that requires Rad51, the histone variant H2A.Z, its SUMO modification, and the DNA-damage checkpoint. Indeed, H2A.Z is deposited close to the break early but transiently and directs DNA resection, single DSB-induced checkpoint activation, and DSB anchoring. Thus, a persistent DSB induces a multifaceted response, which is linked to a specific chromatin mark.
机译：DNA双链断裂（DSB）对细胞具有严重的危害，因为它们会导致基因组不稳定。 DSB修复涉及将修复因子顺序募集到DSB，然后进行Rad51介导的同源性探测，DNA合成和连接。但是，如果没有发现同源性并且DSB持续存在，那么细胞如何反应仍知之甚少。在这里，通过监测单个持续性DNA断裂，我们显示，在进行DNA切除和RPA募集之后，Rad51从DSB双向传播整个染色体，但仅在断裂的染色体上有选择地传播。值得注意的是，持久性DSB随后在需要Rad51，组蛋白变体H2A.Z，其SUMO修饰和DNA损伤检查点的过程中被固定到核外围。实际上，H2A.Z较早但短暂地沉积在断裂附近，并指导DNA切除，单个DSB诱导的检查点激活和DSB锚定。因此，持久性DSB会引发多方面的反应，该反应与特定的染色质标记有关。

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