Abstract

A mutation in the cell division gene ftsK causes super-induction of σ 70-dependent stress defense genes, such as uspA, during entry of cells into stationary phase. In contrast, we report here that stationary phase induction of σ S-dependent genes, uspB and cfa, is attenuated and that σ S accumulates at a lower rate in ftsK1 cells. Ectopic overexpression of rpoS restored induction of the rpoS regulon in the ftsK mutant, as did a deletion in the recA gene. Thus, a mutation in the cell division gene, ftsK, uncouples the otherwise coordinated induction of σ S-dependent genes and the universal stress response gene, uspA, during entry into stationary phase.

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