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首页> 外文期刊>Journal of Molecular Biology >Patching Broken DNA: Nucleosome Dynamics and the Repair of DNA Breaks
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Patching Broken DNA: Nucleosome Dynamics and the Repair of DNA Breaks

机译：修补断裂的DNA：核小体动力学和DNA断裂的修复

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The ability of cells to detect and repair DNA double-strand breaks (DSBs) is dependent on reorganization of the surrounding chromatin structure by chromatin remodeling complexes. These complexes promote access to the site of DNA damage, facilitate processing of the damaged DNA and, importantly, are essential to repackage the repaired DNA. Here, we will review the chromatin remodeling steps that occur immediately after DSB production and that prepare the damaged chromatin template for processing by the DSB repair machinery. DSBs promote rapid accumulation of repressive complexes, including HP1, the NuRD complex, H2A.Z and histone methyltransferases at the DSB. This shift to a repressive chromatin organization may be important to inhibit local transcription and limit mobility of the break and to maintain the DNA ends in close contact. Subsequently, the repressive chromatin is rapidly dismantled through a mechanism involving dynamic exchange of the histone variant H2A.Z. H2A.Z removal at DSBs alters the acidic patch on the nucleosome surface, promoting acetylation of the H4 tail (by the NuA4-Tip60 complex) and shifting the chromatin to a more open structure. Further, H2A.Z removal promotes chromatin ubiquitination and recruitment of additional DSB repair proteins to the break. Modulation of the nucleosome surface and nucleosome function during DSB repair therefore plays a vital role in processing of DNA breaks. Further, the nucleosome surface may function as a central hub during DSB repair, directing specific patterns of histone modification, recruiting DNA repair proteins and modulating chromatin packing during processing of the damaged DNA template. (C) 2015 Elsevier Ltd. All rights reserved.
机译：细胞检测和修复DNA双链断裂（DSB）的能力取决于染色质重塑复合物对周围染色质结构的重组。这些复合物可促进接近DNA损伤位点，促进受损DNA的加工，重要的是，对于重新包装修复后的DNA至关重要。在这里，我们将回顾在DSB生产后立即进行的染色质重塑步骤，这些步骤将准备受损的染色质模板，以供DSB维修机构进行处理。 DSB促进了抑制复合物的快速积累，包括HP1，NuRD复合物，H2A.Z和组蛋白甲基转移酶。这种向抑制性染色质组织的转变对于抑制局部转录并限制断裂的迁移并保持DNA末端紧密接触可能很重要。随后，通过涉及组蛋白变体H2A.Z动态交换的机制迅速消除了抑制性染色质。在DSB处去除H2A.Z会改变核小体表面上的酸性斑块，从而促进H4尾部的乙酰化（通过NuA4-Tip60复合物）并使染色质转移到更开放的结构。此外，H2A.Z的去除促进了染色质的泛素化和其他DSB修复蛋白的募集到断裂。因此，在DSB修复过程中核小体表面和核小体功能的调节在DNA断裂的处理中起着至关重要的作用。此外，核小体表面可在DSB修复过程中充当中心枢纽，指导组蛋白修饰的特定模式，募集DNA修复蛋白并在处理受损的DNA模板期间调节染色质堆积。 （C）2015 Elsevier Ltd.保留所有权利。

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