The Escherichia coli ftsK1 mutation attenuates the induction of sigma(S)-dependent genes upon transition to stationary phase

FEMS Microbiol Lett. 2002 Jan 2;206(1):19-23. doi: 10.1111/j.1574-6968.2002.tb10980.x.

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, ftsK, uncouples the otherwise coordinated induction of sigma(S)-dependent genes and the universal stress response gene, uspA, during entry into stationary phase.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Bacterial Proteins / genetics
  • Bacterial Proteins / metabolism*
  • Cyclopropanes / metabolism
  • Escherichia coli / genetics
  • Escherichia coli / growth & development*
  • Escherichia coli Proteins
  • Fatty Acids / metabolism
  • Gene Deletion
  • Gene Expression Regulation, Bacterial*
  • Membrane Proteins / genetics*
  • Membrane Proteins / metabolism
  • Mutation*
  • Rec A Recombinases / genetics
  • Sigma Factor / genetics
  • Sigma Factor / metabolism*

Substances

  • Bacterial Proteins
  • Cyclopropanes
  • Escherichia coli Proteins
  • Fatty Acids
  • FtsK protein, E coli
  • Membrane Proteins
  • Sigma Factor
  • cyclopropane fatty acids
  • sigma factor KatF protein, Bacteria
  • cyclopropane
  • Rec A Recombinases