Regulation of the heat-shock response in bacteria

Annu Rev Microbiol. 1993;47:321-50. doi: 10.1146/annurev.mi.47.100193.001541.

Abstract

When bacteria cells are exposed to higher temperature, a set of heat-shock proteins (hsps) is induced rapidly and transiently to cope with increased damage in proteins. The mechanism underlying induction of hsps has been a central issue in the heat-shock response and studied intensively in Escherichia coli. Immediately upon temperature upshift, the cellular level of sigma 32 responsible for transcription of heat-shock genes increases rapidly and transiently. The increase in sigma 32 results from both increased synthesis and stabilization of sigma 32, which is ordinarily very unstable. A clue to further understanding of early regulatory events came from recent analysis of translational induction and subsequent shut-off of sigma 32 synthesis. Whereas a 5'-coding region of mRNA for sigma 32 is involved in the induction mediated by the mRNA secondary structure, a distinct segment of sigma 32 polypeptide further downstream is involved in the DnaK/DnaJ-mediated shut-off and destabilization of sigma 32 that may be mutually interconnected.

Publication types

  • Review

MeSH terms

  • Bacteria / genetics*
  • Bacteria / metabolism
  • Base Sequence
  • DNA, Bacterial
  • Gene Expression Regulation, Bacterial
  • Heat-Shock Proteins / genetics*
  • Heat-Shock Proteins / metabolism
  • Molecular Sequence Data
  • RNA, Bacterial
  • Sigma Factor / genetics
  • Sigma Factor / metabolism
  • Transcription Factors*

Substances

  • DNA, Bacterial
  • Heat-Shock Proteins
  • RNA, Bacterial
  • Sigma Factor
  • Transcription Factors
  • heat-shock sigma factor 32