DNA Damage Response Regulation by Histone Ubiquitination.
DNA Damage Response Regulation by Histone Ubiquitination.
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DOI：
10.3390/ijms23158187
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发表时间：
2022-07-25
影响因子：
5.6
通讯作者：
中科院分区：
文献类型：
--
作者：
细胞不断地暴露在大量的基因毒性应激下，导致DNA损伤。DNA双链断裂(DSB)是最严重的损伤之一，应该进行系统的修复以保持基因组的完整性。修复效率与染色质结构密切相关，染色质结构受组蛋白翻译后修饰的调节，包括泛素化。最近的证据表明，组蛋白泛素化和DNA损伤反应之间存在串扰，这表明了DNA修复的系统调控模式。DSB修复有两条主要途径，即非同源末端连接和同源重组，该途径的选择部分受组蛋白翻译后修饰的控制，包括泛素化。组蛋白泛素化改变DSB附近的染色质结构，作为选择和招募修复蛋白的平台；去泛素化酶去除这些修饰会抑制修复蛋白的招募，促进修复反应的收敛。本文对组蛋白泛素化调控的DNA损伤反应进行了全面的综述。
Cells are constantly exposed to numerous genotoxic stresses that induce DNA damage. DNA double-strand breaks (DSBs) are among the most serious damages and should be systematically repaired to preserve genomic integrity. The efficiency of repair is closely associated with chromatin structure, which is regulated by posttranslational modifications of histones, including ubiquitination. Recent evidence shows crosstalk between histone ubiquitination and DNA damage responses, suggesting an integrated model for the systematic regulation of DNA repair. There are two major pathways for DSB repair, viz., nonhomologous end joining and homologous recombination, and the choice of the pathway is partially controlled by posttranslational modifications of histones, including ubiquitination. Histone ubiquitination changes chromatin structure in the vicinity of DSBs and serves as a platform to select and recruit repair proteins; the removal of these modifications by deubiquitinating enzymes suppresses the recruitment of repair proteins and promotes the convergence of repair reactions. This article provides a comprehensive overview of the DNA damage response regulated by histone ubiquitination in response to DSBs.
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