Regulation of the heat-shock response in bacteria

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.