Abstract
A mutation in the cell division gene ftsK causes super-induction of sigma(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 sigma(S)-dependent genes, uspB and cfa, is attenuated and that sigma(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,ftsY, uncouples the otherwise coordinated induction of sigma(S)-dependent genes and the universal stress response gene, uspA, during entry into stationary phase. (C) 2002 Federation of European Microbiological Societies, Published by Elsevier Science B.V. All rights reserved

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