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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >TRF2 is required for repair of nontelomeric DNA double-strand breaks by homologous recombination
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TRF2 is required for repair of nontelomeric DNA double-strand breaks by homologous recombination

机译：TRF2是通过同源重组修复非端粒DNA双链断裂所必需的

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摘要

TRF2 (telomeric repeat binding factor 2) is an essential component of the telomeric cap, where it forms and stabilizes the T-loop junctions. TRF2 forms the T-loops by stimulating strand invasion of the 3' overhang into duplex DNA. TRF2 also has been shown to localize to nontelomeric DNA double-strand breaks , but its functional role in DNA repair has not been examined. Here, we present evidence that TRF2 is involved in homologous recombination (HR) repair of nontelomeric double-strand breaks. Depletion of TRF2 strongly inhibited HR and delayed the formation of Rad51 foci after γ-irradiation, whereas overexpression of TRF2 stimulated HR. Depletion of TRF2 had no effect on nonhomologous end-joining, and overexpression of TRF2 inhibited nonhomologous end-joining. We propose, based on our results and on the ability of TRF2 to mediate strand invasion, that TRF2 plays an essential role in HR by facilitating the formation of early recombination intermediates.
机译：TRF2（端粒重复结合因子2）是端粒帽的重要组成部分，它形成并稳定T环连接。 TRF2通过刺激3'突出端进入双链体DNA的链入侵形成T环。还已经证明TRF2定位于非端粒DNA双链断裂，但是尚未检查其在DNA修复中的功能。在这里，我们提供了TRF2参与非端粒双链断裂的同源重组（HR）修复的证据。 TRF2的耗竭强烈抑制了HR，并延迟了γ射线照射后Rad51灶的形成，而TRF2的过表达刺激了HR。 TRF2的耗尽对非同源末端连接没有影响，而TRF2的过表达抑制了非同源末端连接。根据我们的研究结果和TRF2介导链入侵的能力，我们建议TRF2通过促进早期重组中间体的形成在HR中起重要作用。

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