首页> 外文OA文献 >Oxygen-dependent mutagenesis in Escherichia coli lacking superoxide dismutase.
【2h】

Oxygen-dependent mutagenesis in Escherichia coli lacking superoxide dismutase.

机译:缺乏超氧化物歧化酶的大肠杆菌中的氧依赖性诱变。

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务,本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文,但由于OA文献来源多样且变更频繁,仍可能出现获取不到、文献不完整或与标题不符等情况,如果获取不到我们将提供退款服务。请知悉。

摘要

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.
机译:完全缺乏超氧化物歧化酶(SOD)的大肠杆菌双突变体(sodA sodB)在有氧生长过程中的突变率大大提高。缺乏锰SOD(MnSOD)但具有铁SOD(FeSOD)的单个突变体的增幅较小,而缺乏FeSOD但具有MnSOD的单个突变体的增幅较小。诱变的增强完全取决于氧的存在,增加超氧化物自由基通量的处理会产生更高水平的诱变。过量产生两种形式的SOD的质粒的存在将诱变水平降低至野生型,这表明O2依赖性增强是由于SOD的缺乏所致。诱变的增强是独立于RecA的,并且在有氧生长过程中完全缺乏SOD不会诱导SOS反应。但是,需氧生长的sodA sodB突变体中增强的诱变作用很大程度上取决于功能性核酸外切酶III,这表明超氧化物自由基通量的增加导致可被该酶作用的DNA损伤,从而导致突变。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号