The recovery of stalled replication forks depends on the controlled resection of nascent DNA and on the loading of cohesin. These processes operate in the context of nascent chromatin, but the impact of nucleosome structure on a fork restart remains poorly understood. Here, we show that the Mre11-Rad50-Xrs2 (MRX) complex acts together with the chromatin modifiers Gcn5 and Set1 and the histone remodelers RSC, Chd1, and Isw1 to promote chromatin remodeling at stalled forks. Increased chromatin accessibility facilitates the resection of nascent DNA by the Exo1 nuclease and the Sgs1 and Chl1 DNA helicases. Importantly, increased ssDNA promotes the recruitment of cohesin to arrested forks in a Scc2-Scc4-dependent manner. Altogether, these results indicate that MRX cooperates with chromatin modifiers to orchestrate the action of remodelers, nucleases, and DNA helicases, promoting the resection of nascent DNA and the loading of cohesin, two key processes involved in the recovery of arrested forks.

中文翻译：

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MRX在停滞的复制叉处增加了染色质的可及性，以促进新生的DNA切除和黏附素装载。

停滞的复制叉的恢复取决于新生DNA的受控切除和黏附素的负载。这些过程在新生染色质的背景下进行，但核小体结构对叉重启的影响仍然知之甚少。在这里，我们显示Mre11-Rad50-Xrs2（MRX）复合物与染色质修饰剂Gcn5和Set1以及组蛋白重塑剂RSC，Chd1和Isw1一起起作用，以促进停滞的叉子上的染色质重塑。染色质可及性的提高促进了Exo1核酸酶以及Sgs1和Chl1 DNA解旋酶对新生DNA的切除。重要的是，增加的ssDNA会以Scc2-Scc4依赖的方式促进将粘着素募集至被捕的叉子。总而言之，这些结果表明MRX与染色质修饰剂协同作用来协调重塑剂，核酸酶，