DNA lesions or other barriers frequently compromise replisome progress. The SF2 helicase RecG is a key enzyme in the processing of postreplication gaps or regressed forks in Escherichia coli. A deletion of the recG gene renders cells highly sensitive to a range of DNA damaging agents. Here, we demonstrate that RecG function is at least partially complemented by another SF2 helicase, RadD. A ΔrecGΔradD double mutant exhibits an almost complete growth defect, even in the absence of stress. Suppressors appear quickly, primarily mutations that compromise priA helicase function or recA promoter mutations that reduce recA expression. Deletions of uup (encoding the UvrA-like ABC system Uup), recO, or recF also suppress the ΔrecGΔradD growth phenotype. RadD and RecG appear to avoid toxic situations in DNA metabolism, either resolving or preventing the appearance of DNA repair intermediates produced by RecA or RecA-independent template switching at stalled forks or postreplication gaps. Barriers to replisome progress that require intervention by RadD or RecG occur in virtually every replication cycle. The results highlight the importance of the RadD protein for general chromosome maintenance and repair. They also implicate Uup as a new modulator of RecG function.

中文翻译：

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在每个大肠杆菌复制周期中解决有毒DNA修复中间体：RecG，Uup和RadD的关键作用。

DNA损伤或其他障碍经常损害复制过程。SF2解旋酶RecG是大肠杆菌中复制后间隙或前叉退化过程中的关键酶。recG基因的缺失使细胞对一系列DNA破坏剂高度敏感。在这里，我们证明RecG功能至少部分由另一种SF2解旋酶RadD补充。甲ΔrecGΔradD双重突变体显示出几乎完全的生长缺陷，即使在不存在压力。抑制因子迅速出现，主要是损害priA解旋酶功能的突变或降低recA表达的recA启动子突变。删除uup（编码类似UvrA的ABC系统Uup），recO或recF也可以抑制ΔrecGΔradD生长表型。RadD和RecG似乎可以避免DNA代谢中的毒性情况，从而解决或防止出现由停滞的叉子或复制后间隙处的RecA或独立于RecA的模板切换产生的DNA修复中间体的现象。几乎每个复制周期都会出现需要RadD或RecG干预的复制进度障碍。结果突出了RadD蛋白对于一般染色体维持和修复的重要性。它们还暗示了Uup作为RecG功能的新调制器。