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首页> 外文期刊>Journal of bacteriology >Role of mismatch repair in the Escherichia coli UVM response.
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Role of mismatch repair in the Escherichia coli UVM response.

机译：错配修复在大肠杆菌UVM反应中的作用。

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Mutagenesis at 3,N4-ethenocytosine (epsilonC), a nonpairing mutagenic lesion, is significantly enhanced in Escherichia coli cells pretreated with UV, alkylating agents, or H2O2. This effect, termed UVM (for UV modulation of mutagenesis), is distinct from known DNA damage-inducible responses, such as the SOS response, the adaptive response to alkylating agents, or the oxyR-mediated response to oxidative agents. Here, we have addressed the hypothesis that UVM results from transient depletion of a mismatch repair activity that normally acts to reduce mutagenesis. To test whether the loss of mismatch repair activities results in the predicted constitutive UVM phenotype, E. coli cells defective for methyl-directed mismatch repair, for very-short-patch repair, or for the N-glycosylase activities MutY and MutM were treated with the UVM-inducing agent 1-methyl-3-nitro-1-nitrosoguanidine, with subsequent transfection of M13 viral single-stranded DNA bearing a site-specific epsilonC lesion. Survival of the M13 DNA was measured as transfection efficiency, and mutation fixation at the lesion was characterized by multiplex sequencing technology. The results showed normal UVM induction patterns in all the repair-defective strains tested. In addition, normal UVM induction was observed in cells overexpressing MutH, MutL, or MutS. All strains displayed UVM reactivation, the term used to describe the increased survival of epsilonC-containing DNA in UVM-induced cells. Taken together, these results indicate that the UVM response is independent of known mismatch repair systems in E. coli and may thus represent a previously unrecognized misrepair or misreplication pathway.
机译：在3，N4-乙基胞嘧啶（epsilonC）（一种非配对的诱变病变）处的诱变在经过紫外线，烷化剂或H2O2预处理的大肠杆菌细胞中显着增强。称为UVM（用于诱变的UV调节）的这种效应不同于已知的DNA损伤诱导反应，例如SOS反应，对烷基化剂的适应性反应或oxyR介导的对氧化剂的反应。在这里，我们已经解决了一个假设，即UVM是由于失配修复活性的短暂消耗而引起的，该失配修复活性通常会减少诱变。为了测试错配修复活性的丧失是否导致了预期的本构UVM表型，对处理甲基定向错配修复，极短补丁修复或N-糖基化酶活性缺陷的大肠杆菌细胞MutY和MutM进行了UVM诱导剂1-甲基-3-硝基-1-亚硝基胍，随后转染带有位点特异性ε损伤的M13病毒单链DNA。以转染效率来测量M13 DNA的存活，并通过多重测序技术表征病变处的突变固定。结果显示在所有测试的缺陷修复菌株中正常的UVM诱导模式。此外，在过表达MutH，MutL或MutS的细胞中观察到正常的UVM诱导。所有菌株均显示UVM激活，该术语用于描述UVM诱导的细胞中含有epsilonC的DNA的存活增加。综上所述，这些结果表明，UVM反应独立于大肠杆菌中已知的错配修复系统，因此可能代表以前无法识别的错配或错配途径。

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