DNA damage-induced replication fork regression and processing in Escherichia coli
DNA damage-induced replication fork regression and processing in Escherichia coli
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DOI：
10.1126/science.1081328
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发表时间：
2003-02-14
期刊：
影响因子：
56.9
通讯作者：
Courcelle, CT
中科院分区：
文献类型：
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作者：
Courcelle, J;Donaldson, JR;Courcelle, CT
阻止复制的DNA损伤是所有细胞重排、突变和致死的主要原因。在大肠杆菌中，紫外线（UV）诱导的DNA损伤后，复制恢复需要RecA和其他几种recF途径蛋白。为了表征损伤阻断的复制叉恢复的机制，我们使用二维琼脂糖凝胶电泳显示复制阻断的DNA损伤诱导体内复制叉的瞬时逆转。反向复制叉中间体由RecA和RecF稳定，并且当这些蛋白质不存在时由RecQ-RecJ解旋酶-核酸酶降解。我们认为，分叉退化允许修复酶获得复制阻断病变，允许进行性复制恢复一旦阻断病变被删除。
DNA lesions that block replication are a primary cause of rearrangements, mutations, and lethality in all cells. After ultraviolet (UV)-induced DNA damage in Escherichia coli, replication recovery requires RecA and several other recF pathway proteins. To characterize the mechanism by which lesion-blocked replication forks recover, we used two-dimensional agarose get electrophoresis to show that replication-blocking DNA lesions induce a transient reversal of the replication fork in vivo. The reversed replication fork intermediate is stabilized by RecA and RecF and is degraded by the RecQ-RecJ helicase-nuclease when these proteins are absent. We propose that fork regression allows repair enzymes to gain access to the replication-blocking lesion, allowing processive replication to resume once the blocking lesion is removed.