INDUCTION OF THE SOS RESPONSE BY HYDROGEN-PEROXIDE IN VARIOUS ESCHERICHIA-COLI MUTANTS WITH ALTERED PROTECTION AGAINST OXIDATIVE DNA DAMAGE
INDUCTION OF THE SOS RESPONSE BY HYDROGEN-PEROXIDE IN VARIOUS ESCHERICHIA-COLI MUTANTS WITH ALTERED PROTECTION AGAINST OXIDATIVE DNA DAMAGE
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DOI：
10.1128/jb.171.11.6141-6147.1989
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发表时间：
1989-11-01
影响因子：
3.2
通讯作者：
HOFNUNG, M
中科院分区：
文献类型：
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作者：
GOERLICH, O;QUILLARDET, P;HOFNUNG, M
通过 sfiA::lacZ 操纵子融合在大肠杆菌中测量 H2O2 对 SOS 反应的诱导。研究了参与 DNA 修复或 DNA 代谢的基因突变对 SOS 反应的影响。我们发现，在uvrA突变体中，H2O2在比uvr+亲本菌株中更低的浓度下诱导SOS反应，这表明H2O2诱导的一些损伤可能被uvrABC依赖性切除修复系统修复。第 n 个突变导致胸腺嘧啶二醇 DNA 糖基化酶缺陷，对 SOS 诱导没有可检测到的影响，表明胸腺嘧啶二醇（一种预计由 H2O2 诱导的 DNA 损伤）在我们的条件下不会明显参与该化学物质对 SOS 反应的诱导。在没有 DNA 复制的条件下，H2O2 仍然诱导 dnaC(Ts) uvrA 双突变体的 SOS 反应，表明这种化学物质会诱导 DNA 链断裂。还在各种突变体中检测了 H2O2 诱导的 SOS 反应，这些突变体受到怀疑对氧化应激保护很重要的基因的影响。过氧化氢酶基因 katE 和 katG 的突变仅产生很小的影响。然而，在 oxyR 缺失突变体中，不会发生对 H2O2 的适应性反应，SOS 诱导发生在比 oxyR+ 亲本菌株低得多的 H2O2 浓度下。这些结果表明，在我们的条件下，一些受 oxyR 基因调节的酶对于防止 H2O2 诱导的 DNA 损伤（触发 SOS 反应）比过氧化氢酶更重要。
The induction of the SOS response by H2O2 was measured in Escherichia coli by means of a sfiA::lacZ operon fusion. The effects of mutations in genes involved in DNA repair or DNA metabolism on the SOS response were investigated. We found that in an uvrA mutant, H2O2 induced the SOS response at lower concentrations than in the uvr+ parent strain, indicating that some lesions induced by H2O2 may be repaired by the uvrABC-dependent excision repair system. A nth mutation, yielding deficiency in thymine glycol DNA glycosylase, had no detectable effect on SOS induction, indicating that thymine glycol, a DNA lesion expected to be induced by H2O2, does not participate detectably in the induction of the SOS response by this chemical under our conditions. H2O2 still induced the SOS response in a dnaC(Ts) uvrA double mutant under conditions in which no DNA replication proceeds, suggesting that this chemical induces DNA strand breaks. Induction of the SOS response by H2O2 was also assayed in various mutants affected in genes suspected to be important for protection against oxidative stress. Mutations in the catalase genes, katE and katG, had only minor effects. However, in an oxyR deletion mutant, in which the adaptative response to H2O2 does not occur, SOS induction occurred at much lower H2O2 concentrations than in the oxyR+ parent strain. These results indicate that some enzymes regulated by the oxyR gene are, under our conditions, more important than catalase for protection against the H2O2-induced DNA damages which trigger the SOS response.