Altshuler M
Mutat Res. 1993 Aug;294(2):91-100. doi: 10.1016/0921-8777(93)90017-b.
Following exposure to UV light DNA replication stops and then resumes. The SOS response is required for the restoration of replication. Replication recovery occurs in lexA(Ind) cells carrying a high constitutive level of RecA protein. Replication is also affected by UmuCD proteins, photoreactivation, and excision repair. In addition, there is a constitutive and recA independent way to replicate over UV photoproducts associated with the production of gaps in daughter DNA strands. There are two ways to account for the replication in UV-irradiated cells. A stalled replication fork can be reactivated. Alternatively, a replication fork could be destroyed irreparably, with no available way to complete the round of replication. In that case, postirradiation replication could be due exclusively to replication forks assembled de novo at the origin(s). Changes in replication initiation are observed following UV irradiation. Initiations are first inhibited and then stimulated. They become independent of de novo protein synthesis and sometimes do not stop in dnaA(ts) mutants shifted to 42 degrees C. Although the inducible functions are involved in the recovery of replication at different levels of UV damage, some modifications of the replication initiation mechanism appear to be specific to severely damaged cells. Such modifications seem to include the dnaA(ts) independence for initiations and the transient initiation inhibition. RecA protein can be directly involved both in the modification of initiation and in reactivation of the stalled replication forks. Although the restoration of replication depends on the SOS response a synthesis of some protein(s) that do not belong to the LexA regulon seems to be required as well. These proteins can be under RecA control and one of their functions may be to inhibit the rnhA gene. Certain recA mutations may selectively affect different mechanisms of the replication recovery (namely, recA430, recA727, recA718, recA1730). Overproduction of the photoreactivating enzyme in the dark could influence UmuCD activity in replication. The UmuCD function appears to be blocked in strains carrying the dnaE1026 mutation or overproducing the dnaQ protein. For some unknown reason the UmuCD-associated replication mechanism is the only one available for phage with damaged DNA.
暴露于紫外线后，DNA复制停止，然后恢复。复制的恢复需要SOS应答。在携带高组成水平RecA蛋白的lexA(Ind)细胞中发生复制恢复。复制也受UmuCD蛋白、光复活和切除修复的影响。此外，存在一种组成型且不依赖RecA的方式来越过与子代DNA链中缺口产生相关的紫外线光产物进行复制。有两种方式可以解释紫外线照射细胞中的复制情况。停滞的复制叉可以重新激活。或者，复制叉可能被不可修复地破坏，没有可用的方法完成一轮复制。在这种情况下，照射后复制可能完全归因于在起始位点从头组装的复制叉。紫外线照射后观察到复制起始的变化。起始首先受到抑制，然后受到刺激。它们变得独立于从头蛋白质合成，有时在转移到42摄氏度的dnaA(ts)突变体中不会停止。尽管诱导性功能在不同程度的紫外线损伤下参与复制恢复，但复制起始机制的一些修饰似乎是严重受损细胞特有的。这种修饰似乎包括起始对dnaA(ts)的独立性和短暂的起始抑制。RecA蛋白可以直接参与起始的修饰和停滞复制叉的重新激活。尽管复制的恢复依赖于SOS应答，但似乎也需要一些不属于LexA调控子的蛋白质的合成。这些蛋白质可能受RecA控制，其功能之一可能是抑制rnhA基因。某些recA突变可能选择性地影响复制恢复的不同机制（即recA430、recA727、recA718、recA1730）。黑暗中光复活酶的过量产生可能影响复制中的UmuCD活性。在携带dnaE1026突变或过量产生dnaQ蛋白的菌株中，UmuCD功能似乎被阻断。出于一些未知原因，与UmuCD相关的复制机制是受损DNA噬菌体唯一可用的机制。
