Huang Min, Yang Ye Ran, Sun Xiao Yan, Zhang Ting, Guo Cai Xia
CAS Key Laboratory of Genomics and Precision Medicine, Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing 100101, China.
University of Chinese Academy of Sciences, Beijing 100049, China.
Yi Chuan. 2018 Nov 20;40(11):1007-1014. doi: 10.16288/j.yczz.18-176.
REV1 is one of the major Y-family DNA polymerases. It not only functions as a scaffold protein to mediate other specialized DNA polymerases to sites of lesions, but also inserts deoxycytidine across the lesion strand during translesion DNA synthesis (TLS). Meanwhile, REV1 has been reported to be involved in homologous recombination (HR) repair. Here we further explore the roles of REV1-interacting proteins RAD51 and RAD51C in REV1-mediated DNA double-strand break (DSB) repair. We found that RAD51 but not RAD51C regulates REV1 recruitment to DSB sites via pulsed laser microirradiation. Interestingly, immunofluorescence staining exhibits that REV1 also regulates RAD51 focus formation in response to CPT treatment. These results suggest that REV1 and RAD51 might be mutually dependent on each other in the REV1-related HR pathway.
REV1是主要的Y家族DNA聚合酶之一。它不仅作为一种支架蛋白介导其他特殊的DNA聚合酶到达损伤位点，还在跨损伤DNA合成（TLS）过程中在损伤链对面插入脱氧胞苷。同时，据报道REV1参与同源重组（HR）修复。在这里，我们进一步探讨了与REV1相互作用的蛋白RAD51和RAD51C在REV1介导的DNA双链断裂（DSB）修复中的作用。我们发现，通过脉冲激光微照射，RAD51而非RAD51C调节REV1募集到DSB位点。有趣的是，免疫荧光染色显示，REV1也响应喜树碱（CPT）处理调节RAD51焦点形成。这些结果表明，在与REV1相关的HR途径中，REV1和RAD51可能相互依赖。
