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大肠杆菌中分泌蛋白前体的积累会诱导热休克反应。

Accumulation of secretory protein precursors in Escherichia coli induces the heat shock response.

作者信息

Wild J, Walter W A, Gross C A, Altman E

机构信息

Department of Bacteriology, University of Wisconsin, Madison 53706.

出版信息

J Bacteriol. 1993 Jul;175(13):3992-7. doi: 10.1128/jb.175.13.3992-3997.1993.

DOI:10.1128/jb.175.13.3992-3997.1993
PMID:8320215
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC204827/
Abstract

The accumulation of secretory protein precursors, caused either by mutations in secB or secA or by the overproduction of export-defective proteins, results in a two- to fivefold increase in the synthesis of heat shock proteins. In such strains, sigma 32, the alternative sigma factor responsible for transcription of the heat shock genes, is stabilized. The resultant increase in the level of sigma 32 leads to increased transcription of heat shock genes and increased synthesis of heat shock proteins. We have also found that although a secB null mutant does not grow on rich medium at a temperature range of 30 to 42 degrees C, it does grow at 44 degrees C. In addition, we found that a secB null mutant exhibits greater thermotolerance than the wild-type parental strain. Elevated levels of heat shock proteins, as well as some other non-heat shock proteins, may account for the partial heat resistance of a SecB-lacking strain.

摘要

由secB或secA突变,或由输出缺陷型蛋白质的过量产生所导致的分泌蛋白前体的积累,会使热休克蛋白的合成增加两到五倍。在这类菌株中,负责热休克基因转录的替代σ因子σ32会得到稳定。σ32水平的升高会导致热休克基因转录增加以及热休克蛋白合成增加。我们还发现,虽然secB缺失突变体在30至42摄氏度的丰富培养基上无法生长,但在44摄氏度时却能生长。此外,我们发现secB缺失突变体比野生型亲本菌株表现出更强的耐热性。热休克蛋白以及其他一些非热休克蛋白水平的升高,可能是缺乏SecB的菌株具有部分耐热性的原因。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e71/204827/8d3f66db157b/jbacter00055-0089-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e71/204827/b01972ca2534/jbacter00055-0087-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e71/204827/8486d191e2e8/jbacter00055-0088-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e71/204827/8d3f66db157b/jbacter00055-0089-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e71/204827/b01972ca2534/jbacter00055-0087-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e71/204827/8486d191e2e8/jbacter00055-0088-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e71/204827/8d3f66db157b/jbacter00055-0089-a.jpg

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Accumulation of secretory protein precursors in Escherichia coli induces the heat shock response.大肠杆菌中分泌蛋白前体的积累会诱导热休克反应。
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Heat shock transcription factor σ32 co-opts the signal recognition particle to regulate protein homeostasis in E. coli.热休克转录因子σ32 募集信号识别颗粒以调节大肠杆菌中的蛋白质稳态。
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The synthesis of export-defective proteins can interfere with normal protein export in Escherichia coli.输出缺陷型蛋白质的合成会干扰大肠杆菌中正常的蛋白质输出。
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