Regulation of the Escherichia coli sigma-dependent envelope stress response

Mol Microbiol. 2004 May;52(3):613-9. doi: 10.1111/j.1365-2958.2003.03982.x.


The Escherichia colisigma(E)-dependent stress response pathway controls the expression of genes encoding periplasmic folding catalysts, proteases, biosynthesis enzymes for lipid A (a component of lipopolysaccharide or LPS) and other proteins known or predicted to function in or produce components of the envelope. When E. coli is subjected to heat or other stresses that generate unfolded envelope proteins, sigma(E) activity is induced. Four key players in this signal transduction pathway have been identified: RseA, an inner membrane sigma(E) antisigma factor; RseB, a periplasmic protein that binds to the periplasmic face of RseA; and the DegS and YaeL proteases. The major point of regulation, the interaction between sigma(E) and RseA, is primarily controlled by the stability of RseA. Envelope stress promotes RseA degradation, which occurs by a proteolytic cascade initiated by DegS. There is evidence that one sigma(E)-inducing stress (OmpC overexpression) directly activates DegS to cleave RseA. Secondarily, envelope stress may relieve RseB-mediated enhancement of RseA activity. Additional levels of control upon sigma(E) activity may become evident upon further study of this stress response pathway.

Publication types

  • Review

MeSH terms

  • Animals
  • Escherichia coli / genetics
  • Escherichia coli / metabolism*
  • Escherichia coli Proteins / metabolism*
  • Gene Expression Regulation, Bacterial
  • Heat-Shock Response*
  • Membrane Proteins / metabolism
  • Protein Folding
  • Sigma Factor / metabolism*
  • Signal Transduction
  • Transcription Factors / metabolism*


  • Escherichia coli Proteins
  • Membrane Proteins
  • Sigma Factor
  • Transcription Factors
  • sporulation-specific sigma factors