首页> 美国卫生研究院文献>Journal of Bacteriology >Separate DNA Pol II- and Pol IV-Dependent Pathways of Stress-Induced Mutation during Double-Strand-Break Repair in Escherichia coli Are Controlled by RpoS
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Separate DNA Pol II- and Pol IV-Dependent Pathways of Stress-Induced Mutation during Double-Strand-Break Repair in Escherichia coli Are Controlled by RpoS

机译:RpoS控制大肠埃希氏菌双链断裂修复过程中的应力诱导突变的单独的DNA Pol II和Pol IV依赖性途径受RpoS控制。

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摘要

Previous work showed that about 85% of stress-induced mutations associated with DNA double-strand break repair in carbon-starved Escherichia coli result from error-prone DNA polymerase IV (Pol IV) (DinB) and that the mutagenesis is controlled by the RpoS stress response, which upregulates dinB. We report that the remaining mutagenesis requires high-fidelity Pol II, and that this component also requires RpoS. The results identify a second DNA polymerase contributing to stress-induced mutagenesis and show that RpoS promotes mutagenesis by more than the simple upregulation of dinB.
机译:先前的工作表明,碳缺乏的大肠杆菌中约有85%的应力诱导突变与DNA双链断裂修复有关,是由容易出错的DNA聚合酶IV(Pol IV)(DinB)引起的,诱变由RpoS控制压力反应,上调dinB。我们报告说,剩余的诱变需要高保真Pol II,并且此组件还需要RpoS。结果确定了第二个DNA聚合酶有助于应激诱变,并表明RpoS不仅通过简单上调dinB来促进诱变。

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