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Chromatin remodelling at a DNA double-strand break site in Saccharomyces cerevisiae

机译：酿酒酵母DNA双链断裂位点的染色质重塑

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摘要

The repair of DNA double-strand breaks (DSBs) is crucial for maintaining genome stability. Eukaryotic cells repair DSBs by both non-homologous end joining and homologous recombination. How chromatin structure is altered in response to DSBs and how such alterations influence DSB repair processes are important issues. In vertebrates, phosphorylation of the histone variant H2A.X occurs rapidly after DSB formation, spreads over mega-base chromatin domains, and is required for stable accumulation of repair proteins at damage foci. In Saccharomyces cerevisiae, phosphorylation of the two principal H2A species is also signalled by DSB formation, which spreads ～40 kb in either direction from the DSB. Here we show that near a DSB phosphorylation of H2A is followed by loss of histones H2B and H3 and increased sensitivity of chromatin to digestion by micrococcal nuclease; however, phosphorylation of H2A and nucleosome loss occur independently. The DNA damage sensor MRX is required for histone loss, which also depends on INO80, a nucleosome remodelling complex. The repair protein Rad51 (ref. 6) shows delayed recruitment to DSBs in the absence of histone loss, suggesting that MRX-dependent nucleosome remodelling regulates the accessibility of factors directly involved in DNA repair by homologous recombination. Thus, MRX may regulate two pathways of chromatin changes: nucleosome displacement for efficient recruitment of homologous recombination proteins; and phosphorylation of H2A, which modulates checkpoint responses to DNA damage.
机译：DNA双链断裂（DSB）的修复对于维持基因组稳定性至关重要。真核细胞通过非同源末端连接和同源重组来修复DSB。重要的问题是如何响应于DSB改变染色质结构以及这种改变如何影响DSB修复过程。在脊椎动物中，组蛋白变体H2A.X的磷酸化在DSB形成后迅速发生，分布在兆碱基的染色质域上，是修复蛋白在损伤灶处稳定积累所必需的。在酿酒酵母中，两个主要的H2A物种的磷酸化也通过DSB的形成发出信号，它从DSB的任一方向传播约40 kb。在这里，我们显示H2A在DSB附近发生磷酸化，随后是组蛋白H2B和H3的丢失，以及染色质对微球菌核酸酶消化的敏感性增加。但是，H2A的磷酸化和核小体的丢失是独立发生的。 DNA损伤传感器MRX是组蛋白损失所必需的，这也取决于INO80（一种核小体重塑复合物）。修复蛋白Rad51（参考文献6）显示在没有组蛋白丢失的情况下延迟向DSB募集，表明MRX依赖性核小体重塑调节通过同源重组直接参与DNA修复的因子的可及性。因此，MRX可能调节染色质变化的两个途径：核小体置换以有效募集同源重组蛋白； H2A的磷酸化，调节检查点对DNA损伤的反应。

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  • 来源
    《Nature》 |2005年第7066期|p.379-383|共5页
  • 作者

    Toyoko Tsukuda; Alastair B. Fleming; Jac A. Nickoloff; Mary Ann Osley;

  • 作者单位

    Department of Molecular Genetics and Microbiology, University of New Mexico School of Medicine, 915 Camino de Salud Albuquerque, New Mexico 87131, USA;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 自然科学总论;
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