Acid shock accumulation of sigma S in Salmonella enterica involves increased translation, not regulated degradation
Acid shock accumulation of sigma S in Salmonella enterica involves increased translation, not regulated degradation
复制标题
DOI：
10.1159/000068717
复制
发表时间：
2003-01-01
影响因子：
1.2
通讯作者：
Foster, JW
中科院分区：
文献类型：
--
作者：
Audia, JP;Foster, JW
肠道病原体如肠道沙门氏菌和大肠杆菌面临着艰巨的任务，即通过胃的极酸性pH值存活，以便在宿主肠道中建立感染。这些生物进化出了复杂的应激反应系统，有助于生存。替代性σ因子是S.肠的，并在转录，翻译和蛋白质稳定性水平进行调节。在这些控制机制中，蛋白水解被认为是决定细胞中As水平的最重要因素。在本报告之前，酸休克被认为是通过直接调节降解来增加sigma（S）水平。然而，不能降解as的突变菌株仍然表现出酸休克诱导的as。我们在这里证明，rpoS翻译是酸胁迫控制的主要焦点，并负责观察到的（as水平的增加。构建了一系列rpoS mRNA的566个核苷酸非翻译区的缺失，以检查该调节区在rpoS酸休克诱导中的重要性。从rpoS信息的5'端开始的渐进性缺失产生酸休克控制的交替丧失和恢复。结果表明，竞争茎环结构协同工作，以控制酸休克诱导rpoS。此外，sigma的半衰期响应于酸休克而不变，并且MviA识别蛋白的过表达导致在酸胁迫条件下组成型sigma降解。数据表明，在对数期，随着产量的增加，非应激细胞足以增加蛋白质半衰期。总的来说，这些结果表明，酸休克稳定的作为是通过翻译控制的合成增加的结果，并不涉及的MviA（RssB/SprE）ClpXP降解复合物的活性的变化。因此，组成性降解可以使细胞能够在酸胁迫减轻时重置as的水平。版权所有（C）2003 S. Karger AG，巴塞尔。
Enteric pathogens such as Salmonella enterica and Escherichia coli face the daunting task of surviving passage through the extremely acid pH of the stomach in order to establish an infection in the host intestinal tract. These organisms have evolved elaborate stress response systems that aid in survival. The alternative sigma factor as is a key regulator of many stress responses in S. enterica and is regulated at the levels of transcription, translation, and protein stability. Of these control mechanisms, proteolysis has been considered paramount in determining as levels in the cell. Until the current report, acid shock was thought to increase sigma(S) levels by directly regulating degradation. However, mutant strains unable to degrade as still exhibited acid shock induction of as. We demonstrate here that rpoS translation is a major focus of acid stress control and is responsible for the observed increase in (as levels. A series of deletions of the 566-nucleotide untranslated region of the rpoS mRNA were constructed to examine the importance of this regulatory region in acid shock induction of rpoS. Progressive deletions starting from the 5' end of the rpoS message produced alternating loss and recovery of acid shock control. The results suggest that competing stem-loop structures work in concert to control the acid shock induction of rpoS. Further, the half-life of sigma(s) was unchanged in response to acid shock and overexpression of the MviA recognition protein resulted in constitutive sigma(s) degradation under acid stress conditions. The data indicate that in log phase, nonstressed cells increasing as production is sufficient to increase protein half-life. In toto, these results suggest that acid shock stabilization of as is the result of increased synthesis via translational control and does not involve changes in the activity of the MviA (RssB/SprE) ClpXP degradation complex. Therefore, constitutive degradation may enable the cell to reset the level of as once acid stress is alleviated. Copyright (C) 2003 S. Karger AG, Basel.