RpoS, the stress-response sigma factor, plays a dual role in the regulation of Escherichia coli’s error-prone DNA polymerase

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. In their natural environments bacteria are constantly as-saulted by a variety of stresses that include nutritional depri-vation, temperature fluctuation, desiccation, and exposure to DNA-damaging agents such as UV light and reactive oxygen species. To survive such challenges, bacteria have evolved co-ordinated cellular defense mechanisms, two of which are th