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RpoS, the Stress Response Sigma Factor, Plays a Dual Role in the Regulation of Escherichia coli's Error-Prone DNA Polymerase IV▿

机译:RpoS,应激反应西格玛因子,在大肠杆菌的Error-Prone DNA聚合酶IV的调控中起双重作用

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摘要

RpoS, Escherichia coli's general stress response sigma factor, regulates error-prone DNA polymerase IV (Pol IV) (encoded by the dinB gene). Pol IV is induced in stationary-phase cells, and thereafter, levels of the protein remain elevated for several days of continuous incubation. This induction and persistence in stationary-phase cells are dependent on RpoS. Data presented here show that this regulation is direct via the RpoS-directed transcription of the dinB gene. However, a loss of RpoS also results in a decrease in Pol IV-dependent mutation when Pol IV is overexpressed from an RpoS-independent promoter in exponentially growing cells. The loss of RpoS also increases cell sensitivity to 4-nitroquinoline-1-oxide, indicating that RpoS affects the ability of Pol IV to bypass DNA lesions. Thus, in addition to directly driving the transcription of the dinB gene in stationary-phase cells, RpoS regulates the activity of Pol IV in exponentially growing cells via a second, indirect pathway.
机译:RpoS是大肠杆菌的一般应激反应总和因子,它调节容易出错的DNA聚合酶IV(Pol IV)(由dinB基因编码)。 Pol IV在固定相细胞中诱导,此后,蛋白质的水平在连续培养的数天中保持较高水平。在固定相细胞中的这种诱导和持久性取决于RpoS。此处提供的数据表明该调节是直接通过dinB基因的RpoS定向转录来实现的。但是,RopS的丢失也会导致在以指数方式生长的细胞中从不依赖RpoS的启动子过度表达Pol IV时,降低了Pol IV依赖性突变。 RpoS的丢失还会增加细胞对4-硝基喹啉-1-氧化物的敏感性,表明RpoS影响Pol IV绕过DNA损伤的能力。因此,除了直接驱动固定相细胞中dinB基因的转录外,RpoS还通过第二个间接途径调节指数生长细胞中Pol IV的活性。

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