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鼠伤寒沙门氏菌的耐酸反应涉及关键酸休克蛋白的短暂合成。

The acid tolerance response of Salmonella typhimurium involves transient synthesis of key acid shock proteins.

作者信息

Foster J W

机构信息

Department of Microbiology and Immunology, College of Medicine, University of South Alabama, Mobile 36688.

出版信息

J Bacteriol. 1993 Apr;175(7):1981-7. doi: 10.1128/jb.175.7.1981-1987.1993.

Abstract

Although Salmonella typhimurium prefers neutral-pH environments, it can adapt to survive conditions of severe low-pH stress (pH 3.3). The process, termed the acid tolerance response (ATR), includes two distinct stages. The first stage, called pre-acid shock, is induced at pH 5.8 and involves the production of an inducible pH homeostasis system functional at external pH values below 4.0. The second stage occurs following an acid shock shift to pH 4.5 or below and is called the post-acid shock stage. During this stage of the ATR, 43 acid shock proteins (ASPs) are synthesized. The present data reveal that several ASPs important for pH 3.3 acid tolerance are only transiently produced. Their disappearance after 30 to 40 min of pH 4.4 acid shock coincides with an inability to survive subsequent pH 3.3 acid challenge. Clearly, an essential feature of inducible acid tolerance is an ability to synthesize these key ASPs. The pre-acid shock stage, with its inducible pH homeostasis system, offers the cell an enhanced ability to synthesize ASPs following rapid shifts to conditions below pH 4.0, an external pH that normally prevents ASP synthesis. The data also address possible signals for ASP synthesis. The inducing signal for 22 ASPs appears to be internal acidification, while external pH serves to induce 13 others. Of the 14 transient ASPs, 10 are induced in response to changes in internal pH. Mutations in the fur (ferric uptake regulator) locus that produce an Atr- acid-sensitive phenotype also eliminate induction of six transiently induced ASPs.

摘要

尽管鼠伤寒沙门氏菌更喜欢中性pH环境,但它能够适应在严重的低pH应激(pH 3.3)条件下存活。这个过程被称为耐酸反应(ATR),包括两个不同阶段。第一阶段称为酸前休克,在pH 5.8时诱导产生,涉及产生一种在外部pH值低于4.0时起作用的可诱导pH稳态系统。第二阶段发生在酸休克转变至pH 4.5或更低之后,称为酸后休克阶段。在ATR的这个阶段,会合成43种酸休克蛋白(ASP)。目前的数据表明,几种对pH 3.3耐酸性很重要的ASP只是短暂产生。它们在pH 4.4酸休克30至40分钟后消失,这与无法在随后的pH 3.3酸挑战中存活相吻合。显然,可诱导耐酸性的一个基本特征是能够合成这些关键的ASP。酸前休克阶段及其可诱导的pH稳态系统,使细胞在快速转变至pH 4.0以下的条件(通常会阻止ASP合成的外部pH)后,有增强的能力合成ASP。数据还探讨了ASP合成的可能信号。22种ASP的诱导信号似乎是内部酸化,而外部pH则诱导另外13种。在14种短暂的ASP中,有10种是响应内部pH变化而诱导产生的。在fur(铁摄取调节因子)位点发生的产生Atr-酸敏感表型的突变,也消除了6种短暂诱导的ASP的诱导。

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