Autoinduction of the ompR response regulator by acid shock and control of the Salmonella enterica acid tolerance response
Autoinduction of the ompR response regulator by acid shock and control of the Salmonella enterica acid tolerance response
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DOI：
10.1046/j.1365-2958.2002.02937.x
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发表时间：
2002-06-01
影响因子：
3.6
通讯作者：
Foster, JW
中科院分区：
文献类型：
--
作者：
Bang, IS;Audia, JP;Foster, JW
肠沙门氏菌鼠伤寒血清型在各种宿主和非宿主环境中定期经历酸应激。遭遇非致命性酸应激（pH > 4）会引发一系列生理变化，称为耐酸反应 (ATR)，有助于细胞耐受极低 pH (pH 3)。这些生理变化在对数期和稳定期细胞中有所不同，并由不同的调节蛋白控制。 OmpR 是一种酸诱导的响应调节剂，对稳定相 ATR 至关重要，但对对数相 ATR 则不然。由于 OmpR 还控制酸诱导毒力操纵子 ssrAB 的表达，因此检查了 ompR 的酸休克诱导，以深入了解沙门氏菌如何将毒力与极端酸性 pH 下的存活联系起来。结果表明，酸性 pH 值诱导 ompR 的启动子不同于用于基础表达的启动子。该启动子的转录受到组蛋白样蛋白 H-NS 的抑制，并且需要 OmpR-P 进行诱导。经典的传感器激酶 EnvZ 和乙酰磷酸协同产生自诱导所需的最佳水平的 OmpR-P。尽管野生型细胞中酸诱导的 ompR 表达需要 OmpR-P，但在 H-NS 不存在的情况下，ompR 转录不需要 OmpR。因此，OmpR-P 在自诱导中的作用是帮助抵消 H-NS 的抑制。该证据与新生霉素松弛 DNA 超螺旋也增加 ompR 转录的发现相结合，表明酸应激通过改变局部 DNA 拓扑而不是通过改变 OmpR 的磷酸化状态来诱导 ompR。
Salmonella enterica serovar Typhimurium periodically experiences acid stress in a variety of host and non-host environments. An encounter with non-lethal acid stress (pH > 4) induces an assortment of physiological changes, called the acid tolerance response (ATR), that helps the cell to tolerate extreme low pH (pH 3). These physiological changes differ in log phase and stationary phase cells and are controlled by different regulatory proteins. OmpR is an acid-induced response regulator critical to the stationary phase ATR but not to the log phase ATR. As OmpR also controls the expression of the acid-induced viru-lence operon ssrAB , acid shock induction of ompR was examined to gain insight into how Salmonella links virulence with survival at extreme acid pH. The results indicate that acid pH induces ompR from a promoter different from that used for basal expression. Transcription from this promoter is repressed by the histone-like protein H-NS and requires OmpR-P for induction. The classic sensor kinase EnvZ and acetyl phosphate collaborate to produce the optimum level of OmpR-P needed for autoinduction. Although OmpR-P is required for acid-induced expression of ompR in wild-type cells, OmpR is not needed for ompR transcription in the absence of H-NS. Thus, the role of OmpR-P in autoinduction is to help to counteract repression by H-NS. This evidence, combined with the finding that relaxing DNA supercoiling with novobiocin also increased ompR transcription, suggests that acid stress induces ompR by altering local DNA topology, not by changing the phosphorylation status of OmpR.