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• W1483173983 endingPage "1503" @default.
• W1483173983 startingPage "1494" @default.
• W1483173983 abstract "The link between cell division defects and the induction of the universal stress response is demonstrated to operate via the RecA regulator of the SOS response. An insertion in the cell division gene ftsK upregulates uspA in a recA ‐dependent manner. Unlike true SOS response genes, this upregulation only occurs in growth‐arrested cells and is LexA independent. Thus, besides ppGpp‐dependent starvation signals, DNA aberrations transduce RecA‐dependent signals to the uspA promoter, which only affect the promoter during stasis. Further, we show that ftsK itself, like uspA , is induced in stationary phase and that this induction requires the stringent control modulon rather than activated RecA. Thus, ftsK , like uspA , is regulated by at least two global regulators: ppGpp of the stringent control network and RecA of the SOS modulon. We suggest that UspA is a new bona fide member of the RecA‐dependent DNA protection and repair system, as mutants lacking functional UspA were found to be sensitive to UV irradiation and mitomycin C exposure. Moreover, the UV sensitivity of uspA mutants is enhanced in an additive manner by the ftsK1 mutation." @default.
• W1483173983 created "2016-06-24" @default.
• W1483173983 creator A5031039093 @default.
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• W1483173983 date "2000-06-01" @default.
• W1483173983 modified "2023-10-17" @default.
• W1483173983 title "The universal stress protein A of <i>Escherichia coli</i> is required for resistance to DNA damaging agents and is regulated by a RecA/FtsK‐dependent regulatory pathway" @default.
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• W1483173983 doi "https://doi.org/10.1046/j.1365-2958.2000.01979.x" @default.
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