OXYGEN-DEPENDENT MUTAGENESIS IN ESCHERICHIA-COLI LACKING SUPEROXIDE-DISMUTASE
OXYGEN-DEPENDENT MUTAGENESIS IN ESCHERICHIA-COLI LACKING SUPEROXIDE-DISMUTASE
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DOI：
10.1073/pnas.83.21.8268
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发表时间：
1986-11-01
影响因子：
11.1
通讯作者：
TOUATI, D
中科院分区：
文献类型：
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作者：
FARR, SB;DARI, R;TOUATI, D
完全缺乏超氧化物歧化酶（SOD）的大肠杆菌双突变体（sodA - sodB）在有氧生长过程中显著提高了突变率。缺乏锰超氧化物歧化酶（MnSOD）而拥有铁超氧化物歧化酶（FeSOD）的单突变体增加幅度较小，而缺乏FeSOD而拥有MnSOD的单突变体则没有这种增加。诱变的增强完全依赖于氧的存在，而增加超氧自由基通量的处理会产生更高水平的诱变。质粒过量产生任何一种形式的超氧化物歧化酶（SOD），会使诱变水平降低到野生型的水平，表明o2依赖性增强是由于缺乏超氧化物歧化酶（SOD）造成的。诱变的增强与reca无关，在有氧生长过程中，SOD的完全缺乏不会诱导SOS反应。然而，在有氧生长的sodA - sodB突变体中，增强的诱变在很大程度上依赖于功能性外切酶III，这表明超氧自由基通量的增加导致DNA损伤，而这种酶可以作用于DNA损伤，从而导致突变。
Escherichia coli double mutants (sodA sodB) completely lacking superoxide dismutase (SOD) have greatly enhanced mutation rates during aerobic growth. Single mutants lacking manganese SOD (MnSOD) but possessing iron SOD (FeSOD) have a smaller increase, and single mutants lacking FeSOD but possessing MnSOD do not show such an increase. The enhancement of mutagenesis is completely dependent on the presence of oxygen, and treatments that increase the flux of superoxide radicals produce even higher levels of mutagenesis. The presence of a plasmid overproducing either form of SOD reduces the level of mutagenesis to that of wild type, showing that the O2-dependent enhancement results from a lack of SOD. The enhancement of mutagenesis is RecA-independent, and a complete lack of SOD does not induce the SOS response during aerobic growth. However, the enhanced mutagenesis in aerobically grown sodA sodB mutants is largely dependent on functional exonuclease III, suggesting that the increased flux of superoxide radicals results in DNA lesions that can be acted on by this enzyme, leading to mutations.