REGULATION OF THE HEAT-SHOCK RESPONSE IN BACTERIA

被引：299

作者：

YURA, T ^{[1
]}

NAGAI, H ^{[1
]}

MORI, H ^{[1
]}

机构：

[1] NATL INST GENET, MISHIMA, SHIZUOKA 411, JAPAN

来源：

ANNUAL REVIEW OF MICROBIOLOGY | 1993年 / 47卷

关键词：

HEAT-SHOCK PROTEIN; STRESS RESPONSE; SIGMA-FACTOR; TRANSLATIONAL CONTROL; ESCHERICHIA-COLI;

D O I：

10.1146/annurev.mi.47.100193.001541

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

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 sigma32 responsible for transcription of heat-shock genes increases rapidly and transiently. This increase in sigma32 results from both increased synthesis and stabilization of sigma32, 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 sigma32 synthesis. Whereas a 5'-coding region of mRNA for sigma32 is involved in the induction meditated by the mRNA secondary structure, a distinct segment of cr 32 polypeptide further downstream is involved in the DnaK/DnaJ-mediated shut-off and destabilization of sigma32 that may be mutually interconnected.

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页码：321 / 350

页数：30

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