DNA 双链断裂处的染色质重塑。
Chromatin remodeling at DNA double-strand breaks.
机构信息
Division of Genomic Stability and DNA Repair, Department of Radiation Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA.
出版信息
Cell. 2013 Mar 14;152(6):1344-54. doi: 10.1016/j.cell.2013.02.011.
Abstract
DNA double-strand breaks (DSBs) can arise from multiple sources, including exposure to ionizing radiation. The repair of DSBs involves both posttranslational modification of nucleosomes and concentration of DNA-repair proteins at the site of damage. Consequently, nucleosome packing and chromatin architecture surrounding the DSB may limit the ability of the DNA-damage response to access and repair the break. Here, we review early chromatin-based events that promote the formation of open, relaxed chromatin structures at DSBs and that allow the DNA-repair machinery to access the spatially confined region surrounding the DSB, thereby facilitating mammalian DSB repair.
摘要
DNA 双链断裂 (DSBs) 可以由多种来源引起，包括暴露于电离辐射中。DSB 的修复涉及核小体的翻译后修饰以及 DNA 修复蛋白在损伤部位的浓缩。因此，DSB 周围核小体的包装和染色质结构可能会限制 DNA 损伤反应的能力，使其无法进入和修复断裂。在这里，我们回顾了早期基于染色质的事件，这些事件促进了 DSB 处开放、松弛的染色质结构的形成，并允许 DNA 修复机制进入 DSB 周围空间受限的区域，从而促进了哺乳动物 DSB 的修复。
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