Regulation of the heat-shock response in bacteria.
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.
Yura
T
T
Institute for Virus Research, Kyoto University, Japan.
Nagai
H
H
Mori
H
H
D001419:Bacteria / Q000235:genetics* / Q000378:metabolism; D001483:Base Sequence; D004269:DNA, Bacterial; D015964:Gene Expression Regulation, Bacterial; D006360:Heat-Shock Proteins / Q000235:genetics* / Q000378:metabolism; D008969:Molecular Sequence Data; D012329:RNA, Bacterial; D012808:Sigma Factor / Q000235:genetics / Q000378:metabolism; D014157:Transcription Factors
D004269:DNA, Bacterial; D006360:Heat-Shock Proteins; D012329:RNA, Bacterial; D012808:Sigma Factor; D014157:Transcription Factors; C069774:heat-shock sigma factor 32