Courcelle J, Crowley D J, Hanawalt P C
Department of Biological Sciences, Stanford University, Stanford, California 94305, USA.
J Bacteriol. 1999 Feb;181(3):916-22. doi: 10.1128/JB.181.3.916-922.1999.
After UV doses that disrupt DNA replication, the recovery of replication at replication forks in Escherichia coli requires a functional copy of the recF gene. In recF mutants, replication fails to recover and extensive degradation of the nascent DNA occurs, suggesting that recF function is needed to stabilize the disrupted replication forks and facilitate the process of recovery. We show here that the ability of recF to promote the recovery of replication requires that the disrupting lesions be removed. In the absence of excision repair, recF+ cells protect the nascent DNA at replication forks, but replication does not resume. The classical view is that recombination proteins operate in pathways that are independent from DNA repair, and therefore the functions of Rec proteins have been studied in repair-deficient cells. However, mutations in either uvr or recF result in failure to recover replication at UV doses from which wild-type cells recover efficiently, suggesting that recF and excision repair contribute to a common pathway in the recovery of replication.
在紫外线剂量破坏DNA复制后，大肠杆菌复制叉处复制的恢复需要recF基因的功能性拷贝。在recF突变体中，复制无法恢复，新生DNA会发生广泛降解，这表明recF功能对于稳定被破坏的复制叉和促进恢复过程是必需的。我们在此表明，recF促进复制恢复的能力要求去除破坏损伤。在缺乏切除修复的情况下，recF⁺细胞保护复制叉处的新生DNA，但复制不会恢复。传统观点认为重组蛋白在与DNA修复无关的途径中起作用，因此Rec蛋白的功能已在修复缺陷细胞中进行了研究。然而，uvr或recF中的突变导致在野生型细胞能有效恢复的紫外线剂量下无法恢复复制，这表明recF和切除修复在复制恢复中共同作用于一条途径。
