RecO acts with RecF and RecR to protect and maintain replication forks blocked by UV-induced DNA damage in Escherichia coli
RecO acts with RecF and RecR to protect and maintain replication forks blocked by UV-induced DNA damage in Escherichia coli
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DOI：
10.1074/jbc.m311012200
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发表时间：
2004-01-30
影响因子：
4.8
通讯作者：
Courcelle, J
中科院分区：
文献类型：
--
作者：
Chow, KH;Courcelle, J
在大肠杆菌中，recF和recR是稳定和维持被UV诱导的DNA损伤所阻止的复制叉所必需的。在不存在RecF的情况下，复制无法恢复，并且被捕的复制叉的新生滞后链被RecQ解旋酶和RecJ核酸酶广泛降解。recO突变体与recF和recR在DNA损伤后的重组和存活测定方面是上位性的。在这项研究中，我们表明，RecO功能与RecF和RecR，以保护新生的滞后链逮捕复制叉后，紫外线照射。在不存在RecO的情况下，在被捕获的复制叉处的新生DNA被广泛降解，并且复制无法恢复。新生DNA降解的程度在recF、recO或recR的单突变体、双突变体或三突变体中是等同的，并且降解依赖于RecJ和RecQ功能。由于RecF已被证明可以保护新生的滞后链免于降解，这些观察结果表明RecR和RecO与RecF一起发挥作用，以保护被捕复制叉的相同新生链，并且可能在恢复过程中的共同点起作用。我们讨论了这些结果有关的RecF，RecO，和RecR的生化和细胞特性和其潜在的作用，在加载RecA丝，以维持复制叉结构后，逮捕复制UV诱导的DNA损伤。
In Escherichia coli, recF and recR are required to stabilize and maintain replication forks arrested by UV-induced DNA damage. In the absence of RecF, replication fails to recover, and the nascent lagging strand of the arrested replication fork is extensively degraded by the RecQ helicase and RecJ nuclease. recO mutants are epistatic with recF and recR with respect to recombination and survival assays after DNA damage. In this study, we show that RecO functions with RecF and RecR to protect the nascent lagging strand of arrested replication forks after UV-irradiation. In the absence of RecO, the nascent DNA at arrested replication forks is extensively degraded and replication fails to recover. The extent of nascent DNA degradation is equivalent in single, double, or triple mutants of recF, recO, or recR, and the degradation is dependent upon RecJ and RecQ functions. Because RecF has been shown to protect the nascent lagging strand from degradation, these observations indicate that RecR and RecO function with RecF to protect the same nascent strand of the arrested replication fork and are likely to act at a common point during the recovery process. We discuss these results in relation to the biochemical and cellular properties of RecF, RecO, and RecR and their potential role in loading RecA filaments to maintain the replication fork structure after the arrest of replication by UV-induced DNA damage.