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首页> 外文期刊>Journal of bacteriology >Cellular Characterization of the Primosome and Rep Helicase in Processing and Restoration of Replication following Arrest by UV-Induced DNA Damage in Escherichia coli
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Cellular Characterization of the Primosome and Rep Helicase in Processing and Restoration of Replication following Arrest by UV-Induced DNA Damage in Escherichia coli

机译：在大肠杆菌中紫外线诱导的DNA损伤被捕后，加工和恢复复制过程中长体和Rep解旋酶的细胞特征

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Following arrest by UV-induced DNA damage, replication is restored through a sequence of steps that involve partial resection of the nascent DNA by RecJ and RecQ, branch migration and processing of the fork DNA surrounding the lesion by RecA and RecF-O-R, and resumption of DNA synthesis once the blocking lesion has been repaired or bypassed. In vitro, the primosomal proteins (PriA, PriB, and PriC) and Rep are capable of initiating replication from synthetic DNA fork structures, and they have been proposed to catalyze these events when replication is disrupted by certain impediments in vivo. Here, we characterized the role that PriA, PriB, PriC, and Rep have in processing and restoring replication forks following arrest by UV-induced DNA damage. We show that the partial degradation and processing of the arrested replication fork occurs normally in both rep and primosome mutants. In each mutant, the nascent degradation ceases and DNA synthesis initially resumes in a timely manner, but the recovery then stalls in the absence of PriA, PriB, or Rep. The results demonstrate a role for the primosome and Rep helicase in overcoming replication forks arrested by UV-induced damage in vivo and suggest that these proteins are required for the stability and efficiency of the replisome when DNA synthesis resumes but not to initiate de novo replication downstream of the lesion.
机译：在被紫外线诱导的DNA损伤阻止后，通过一系列步骤恢复复制，这些步骤包括通过RecJ和RecQ对新生DNA进行部分切除，通过RecA和RecF-OR进行分支迁移和病变周围叉子DNA的加工以及恢复一旦修复或绕过了阻塞性病变，即可完成DNA合成。 在体外，原始蛋白（PriA，PriB和PriC）和Rep能够从合成的DNA叉子结构启动复制，并且有人提出，当复制受到某些障碍的干扰时，它们可以催化这些事件。 体内。在这里，我们描述了PriA，PriB，PriC和Rep在被紫外线诱导的DNA损伤阻止后在处理和还原复制叉中所起的作用。我们表明被逮捕的复制叉的部分降解和处理通常在 rep 和primosome突变体中发生。在每个突变体中，新生的降解停止，DNA合成首先及时恢复，但是随后在没有PriA，PriB或Rep的情况下恢复停滞。结果证明了primosome和Rep解旋酶在克服被阻止的复制叉中的作用由紫外线诱导的体内损伤的研究表明，这些蛋白对于DNA合成恢复时复制体的稳定性和效率是必需的，而不是在其下游启动从头复制。病变。

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