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
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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DOI：
10.1128/jb.00570-10
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发表时间：
2010-09-01
影响因子：
3.2
通讯作者：
Hastings, P. J.
中科院分区：
文献类型：
--
作者：
Frisch, Ryan L.;Su, Yang;Hastings, P. J.
先前的工作表明，在碳饥饿的大肠杆菌中，约85%的与DNA双链断裂修复相关的应激诱导突变是由易错DNA聚合酶IV（Pol IV）（DinB）引起的，并且该诱变是由RpoS应激反应控制的，RpoS应激反应上调DinB。我们报告说，其余的诱变需要高保真Pol II，并且该组件还需要RpoS。结果确定了第二个DNA聚合酶有助于应力诱导的诱变，并表明RpoS促进诱变比简单的上调dinB。
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.