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首页> 外文期刊>Molecular Microbiology >Global analysis of tolerance to secretin-induced stress in Yersinia enterocolitica suggests that the phage-shock-protein system may be a remarkably self-contained stress response.
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Global analysis of tolerance to secretin-induced stress in Yersinia enterocolitica suggests that the phage-shock-protein system may be a remarkably self-contained stress response.

机译：对小肠结肠炎耶尔森氏菌分泌素诱导的压力的耐受性的全球分析表明，噬菌体-休克蛋白系统可能是一个非常独立的应激反应。

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摘要

The phage-shock-protein (Psp) system is essential for Yersinia enterocolitica virulence. Mislocalized secretins induce psp gene expression, and kill psp null strains. We used transposon mutagenesis to investigate whether other genes are required to tolerate secretin-induced stress. Our motivation included the possibility of identifying signal transducers required to activate psp gene expression. Besides Psp, only defects in the RpoE system and the TrkA potassium transporter caused secretin sensitivity. These mutations did not cause the same specific/severe sensitivity as defects in the Psp system, nor did they affect psp gene expression. The Escherichia coli Psp system was reported to be induced via the ArcB redox sensor and to activate anaerobic metabolism. Our screen did not identify arcB, or any genes involved in anaerobic metabolism/regulation. Therefore, we investigated the role of ArcB in Y. enterocolitica and E. coli. ArcB was not required for secretin-dependent induction of psp gene expression.Furthermore, microarray analysis uncovered a restricted transcriptional response to prolonged secretin stress in Y. enterocolitica. Taken together, these data do not support the proposal that the Psp system is induced via ArcB and activates anaerobic metabolism. Rather, they suggest that Psp proteins may sense an inducing trigger and mediate their physiological output(s) directly.
机译：噬菌体休克蛋白（Psp）系统对于小肠结肠炎耶尔森氏菌毒力至关重要。失调的促胰液素诱导psp基因表达，并杀死psp null株。我们使用转座子诱变来研究是否需要其他基因来耐受促胰液素诱导的应激。我们的动机包括发现激活psp基因表达所需的信号转导子的可能性。除Psp之外，仅RpoE系统和TrkA钾转运蛋白中的缺陷引起分泌蛋白敏感性。这些突变不会引起与Psp系统缺陷相同的特异性/严重敏感性，也不会影响psp基因表达。据报道，大肠杆菌Psp系统是通过ArcB氧化还原传感器诱导的，并激活厌氧代谢。我们的筛查未发现arcB或任何与厌氧代谢/调节有关的基因。因此，我们调查了ArcB在小肠结肠炎耶尔森氏菌和大肠杆菌中的作用。分泌素依赖性psp基因表达的诱导不需要ArcB。此外，微阵列分析发现肠球菌中对长期分泌素应激的转录反应受到限制。综上所述，这些数据不支持通过ArcB诱导Psp系统并激活厌氧代谢的建议。相反，他们认为Psp蛋白可能会感应诱导触发并直接介导其生理输出。

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