RNase L facilitates the repair of DNA double‐strand breaks through the nonhomologous end‐joining pathway
RNase L facilitates the repair of DNA double‐strand breaks through the nonhomologous end‐joining pathway
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DOI：
10.1002/1873-3468.13426
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发表时间：
2019-06
期刊：
影响因子：
3.5
通讯作者：
Yiran Zhong;Bingxin Pan;Jie Zhu;Hanjiang Fu;Xiaofei Zheng
中科院分区：
文献类型：
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作者：
Yiran Zhong;Bingxin Pan;Jie Zhu;Hanjiang Fu;Xiaofei Zheng
RNA分子已被发现在DNA双链断裂（DSB）修复中发挥重要作用，但确切的潜在机制仍不清楚。本文旨在阐明脊椎动物免疫系统中重要的核糖核酸酶RNase L在DSB修复中的作用。RNase L的敲低降低了电离辐射或喜树碱诱导DSB后的细胞存活率，并导致DSB修复显著减少，如组蛋白H2AX对Ser139（γH2AX）的磷酸化程度增加和γH2AX核灶形成所证明的。因此，我们的研究结果表明，RNase L与参与DNA末端连接的核心因子（如XRCC4和Lig4）相互作用，并通过非同源末端连接途径促进DSB修复。
RNA molecules have been found to play important roles in DNA double‐strand break (DSB) repair, but the exact underlying mechanism remains unclear. Here, we aimed to clarify the function of RNase L, an important ribonuclease in the immune system of vertebrates, in DSB repair. Knockdown of RNase L reduces cell survival after induction of DSBs by ionizing radiation or camptothecin and causes a significant decrease in DSB repair, as evidenced by an increase in the extent of phosphorylation of histone H2AX on Ser139 (γH2AX) and γH2AX nuclear foci formation. Thus, our findings indicate that RNase L interacts with the core factors involved in DNA end joining, such as XRCC4 and Lig4, and facilitates DSB repair through the nonhomologous end‐joining pathway.