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首页> 外文期刊>Molecular cell >The DNA Translocase FANCM/MHF Promotes Replication Traverse of DNA Interstrand Crosslinks
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The DNA Translocase FANCM/MHF Promotes Replication Traverse of DNA Interstrand Crosslinks

机译：DNA转运酶FANCM / MHF促进DNA链间交联的复制遍历

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The replicative machinery encounters many impediments, some of which can be overcome by lesion bypass or replication restart pathways, leaving repair for a later time. However, interstrand crosslinks (ICLs), which preclude DNA unwinding, are considered absolute blocks to replication. Current models suggest that fork collisions, either from one or both sides of an ICL, initiate repair processes required for resumption of replication. To test these proposals, we developed a single-molecule technique for visualizing encounters of replication forks with ICLs as they occur in living cells. Surprisingly, the most frequent patterns were consistent with replication traverse of an ICL, without lesion repair. The traverse frequency was strongly reduced by inactivation of the translocase and DNA binding activities of the FANCM/MHF complex. The results indicate that translocase-based mechanisms enable DNA synthesis to continue past ICLs and that these lesions are not always absolute blocks to replication.
机译：复制机制遇到许多障碍，可以通过病灶旁路或复制重启途径来克服其中的一些障碍，并在以后进行修复。但是，阻止DNA展开的链间交联（ICL）被视为复制的绝对障碍。当前模型表明，从ICL的一侧或两侧发生的分叉冲突会引发恢复复制所需的修复过程。为了测试这些建议，我们开发了一种单分子技术来可视化ICL在活细胞中发生的复制叉的遭遇。出人意料的是，最常见的模式与ICL的复制遍历一致，而没有病变修复。遍历频率因FANCM / MHF复合物的转位酶失活和DNA结合活性而大大降低。结果表明基于转位酶的机制使DNA合成能够继续通过ICL，并且这些病变并不总是复制的绝对障碍。

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