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乙酸诱导的酸耐受性反应过程中大肠杆菌基因表达的全局分析。

Global analysis of Escherichia coli gene expression during the acetate-induced acid tolerance response.

作者信息

Arnold C N, McElhanon J, Lee A, Leonhart R, Siegele D A

机构信息

Department of Biology, Texas A&M University, College Station, Texas 77843-3258, USA.

出版信息

J Bacteriol. 2001 Apr;183(7):2178-86. doi: 10.1128/JB.183.7.2178-2186.2001.

DOI:10.1128/JB.183.7.2178-2186.2001
PMID:11244055
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC95122/
Abstract

The ability of Escherichia coli to survive at low pH is strongly affected by environmental factors, such as composition of the growth medium and growth phase. Exposure to short-chain fatty acids, such as acetate, proprionate, and butyrate, at neutral or nearly neutral pH has also been shown to increase acid survival of E. coli and Salmonella enterica serovar Typhimurium. To investigate the basis for acetate-induced acid tolerance in E. coli O157:H7, genes whose expression was altered by exposure to acetate were identified using gene arrays. The expression of 60 genes was reduced by at least twofold; of these, 48 encode components of the transcription-translation machinery. Expression of 26 genes increased twofold or greater following treatment with acetate. This included six genes whose products are known to be important for survival at low pH. Five of these genes, as well as six other acetate-induced genes, are members of the E. coli RpoS regulon. RpoS, the stress sigma factor, is known to be required for acid tolerance induced by growth at nonlethal low pH or by entry into stationary phase. Disruption of the rpoS gene by a transposon insertion mutation also prevented acetate-induced acid tolerance. However, induction of RpoS expression did not appear to be sufficient to activate the acid tolerance response. Treatment with either NaCl or sodium acetate (pH 7.0) increased expression of an rpoS::lacZ fusion protein, but only treatment with acetate increased acid survival.

摘要

大肠杆菌在低pH值环境下的生存能力受到多种环境因素的强烈影响,如生长培养基的组成和生长阶段。在中性或接近中性pH值条件下,暴露于短链脂肪酸(如乙酸盐、丙酸盐和丁酸盐)也已被证明可提高大肠杆菌和鼠伤寒沙门氏菌的耐酸性。为了研究乙酸盐诱导大肠杆菌O157:H7耐酸性的基础,利用基因芯片鉴定了因暴露于乙酸盐而表达发生改变的基因。60个基因的表达至少降低了两倍;其中,48个编码转录-翻译机制的组分。用乙酸盐处理后,26个基因的表达增加了两倍或更多。这包括6个已知其产物对低pH值下生存很重要的基因。其中5个基因以及其他6个乙酸盐诱导的基因是大肠杆菌RpoS调控子的成员。RpoS是应激σ因子,已知在非致死性低pH值下生长或进入稳定期诱导的耐酸性中是必需的。转座子插入突变破坏rpoS基因也阻止了乙酸盐诱导的耐酸性。然而,RpoS表达的诱导似乎不足以激活耐酸性反应。用NaCl或乙酸钠(pH 7.0)处理均可增加rpoS::lacZ融合蛋白的表达,但只有用乙酸盐处理可提高耐酸性。

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