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大肠杆菌rpoH(htpR)突变的抑制:suhA回复突变体中的热休克反应

Suppression of rpoH (htpR) mutations of Escherichia coli: heat shock response in suhA revertants.

作者信息

Tobe T, Kusukawa N, Yura T

出版信息

J Bacteriol. 1987 Sep;169(9):4128-34. doi: 10.1128/jb.169.9.4128-4134.1987.

Abstract

Temperature-resistant pseudorevertants were isolated from rpoH (htpR) mutants of Escherichia coli K-12 that cannot grow at a high temperature owing to a deficiency in sigma 32 required for the induction of heat shock proteins. Among them was a class of revertants carrying a suppressor mutation, designated suhA, that suppressed all the nonsense and missense rpoH mutations tested. suhA is located at 77 min, about 1 min away from rpoH, on the genetic map. In contrast to the rpoH mutants, the suhA revertants that contained both rpoH (nonsense) and suhA mutations were fully or partially proficient in the induction of heat shock proteins upon exposure to a high temperature. Under these conditions, transcription from two heat shock promoters as determined by operon fusion was transiently activated. In one of the rpoH(Am) suhA revertants studied in detail, an increase in temperature caused the synthesis of significant amounts of sigma 32, accompanied by increased stability and accumulation of rpoH mRNAs. On the other hand, the same mutation (suhA6) only weakly suppressed the rpoH deletion mutant; however, two of the major heat shock genes, dnaK and groE, were apparently induced in the absence of sigma 32. Thus, suhA6 seems to bring about the induction of heat shock genes by at least two mechanisms, one increasing the level of sigma 32 synthesis, and the other activating some transcription factor other than sigma 32.

摘要

从大肠杆菌K-12的rpoH(htpR)突变体中分离出了耐热性假回复突变体,这些突变体由于热休克蛋白诱导所需的σ32缺乏而无法在高温下生长。其中一类回复突变体携带一个名为suhA的抑制突变,它能抑制所有测试的无义突变和错义rpoH突变。在遗传图谱上,suhA位于77分钟处,距离rpoH约1分钟。与rpoH突变体不同,同时含有rpoH(无义)和suhA突变的suhA回复突变体在暴露于高温时,能完全或部分地正常诱导热休克蛋白。在这些条件下,通过操纵子融合测定的两个热休克启动子的转录被短暂激活。在一个经过详细研究的rpoH(Am)suhA回复突变体中,温度升高导致大量σ32的合成,同时rpoH mRNA的稳定性和积累增加。另一方面,相同的突变(suhA6)对rpoH缺失突变体的抑制作用较弱;然而,两个主要的热休克基因dnaK和groE在没有σ32的情况下明显被诱导。因此,suhA6似乎至少通过两种机制导致热休克基因的诱导,一种是增加σ32的合成水平,另一种是激活除σ32之外的一些转录因子。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cfa0/213719/179f3a0d0a93/jbacter00199-0276-a.jpg

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