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热应激下控制细胞裂解的机制及稳定期的细胞存活策略

Mechanism to control the cell lysis and the cell survival strategy in stationary phase under heat stress.

作者信息

Noor Rashed

机构信息

Department of Microbiology, Stamford University Bangladesh, 51 Siddeswari Road, Dhaka, 1217 Bangladesh.

出版信息

Springerplus. 2015 Oct 13;4:599. doi: 10.1186/s40064-015-1415-7. eCollection 2015.

DOI:10.1186/s40064-015-1415-7
PMID:26543734
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4627973/
Abstract

An array of stress signals triggering the bacterial cellular stress response is well known in Escherichia coli and other bacteria. Heat stress is usually sensed through the misfolded outer membrane porin (OMP) precursors in the periplasm, resulting in the activation of σ(E) (encoded by rpoE), which binds to RNA polymerase to start the transcription of genes required for responding against the heat stress signal. At the elevated temperatures, σ(E) also serves as the transcription factor for σ(H) (the main heat shock sigma factor, encoded by rpoH), which is involved in the expression of several genes whose products deal with the cytoplasmic unfolded proteins. Besides, oxidative stress in form of the reactive oxygen species (ROS) that accumulate due to heat stress, has been found to give rise to viable but non-culturable (VBNC) cells at the early stationary phase, which is in turn lysed by the σ(E)-dependent process. Such lysis of the defective cells may generate nutrients for the remaining population to survive with the capacity of formation of colony forming units (CFUs). σ(H) is also known to regulate the transcription of the major heat shock proteins (HSPs) required for heat shock response (HSR) resulting in cellular survival. Present review concentrated on the cellular survival against heat stress employing the harmonized impact of σ(E) and σ(H) regulons and the HSPs as well as their inter connectivity towards the maintenance of cellular survival.

摘要

一系列触发细菌细胞应激反应的应激信号在大肠杆菌和其他细菌中是众所周知的。热应激通常通过周质中错误折叠的外膜孔蛋白(OMP)前体来感知,从而导致σ(E)(由rpoE编码)的激活,σ(E)与RNA聚合酶结合以启动应对热应激信号所需基因的转录。在高温下,σ(E)还作为σ(H)(主要的热休克西格玛因子,由rpoH编码)的转录因子,σ(H)参与几种基因的表达,其产物处理细胞质中未折叠的蛋白质。此外,已发现由于热应激而积累的活性氧(ROS)形式的氧化应激在早期稳定期产生活的但不可培养(VBNC)细胞,这些细胞又通过σ(E)依赖性过程被裂解。有缺陷细胞的这种裂解可能为其余群体产生营养物质,使其能够以形成菌落形成单位(CFU)的能力存活。已知σ(H)还调节热休克反应(HSR)所需的主要热休克蛋白(HSP)的转录,从而导致细胞存活。本综述集中于利用σ(E)和σ(H)调控子以及HSP的协调作用及其对维持细胞存活的相互连接来实现细胞对热应激的存活。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5006/4627973/b9cd68c3487b/40064_2015_1415_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5006/4627973/a97856f9fedc/40064_2015_1415_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5006/4627973/6bcfb89d1b87/40064_2015_1415_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5006/4627973/b71f629c2e7c/40064_2015_1415_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5006/4627973/fae4f7cee43e/40064_2015_1415_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5006/4627973/b9cd68c3487b/40064_2015_1415_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5006/4627973/a97856f9fedc/40064_2015_1415_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5006/4627973/6bcfb89d1b87/40064_2015_1415_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5006/4627973/b71f629c2e7c/40064_2015_1415_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5006/4627973/fae4f7cee43e/40064_2015_1415_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5006/4627973/b9cd68c3487b/40064_2015_1415_Fig5_HTML.jpg

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