Bacterial survive and respond to adverse changes in the environment by regulating gene transcription through two-component regulatory systems. In Salmonella Typhimurium the STM1485 gene expression is induced under low pH (4.5) during replication inside the epithelial host cell, but it is not involved in sensing or resisting to this condition. Since the RcsCDB system is activated under acidic conditions, we investigated whether this system is able to modulate STM1485 expression. We demonstrated that acid-induced activation of the RcsB represses STM1485 transcription by directly binding to the promoter. Under the same condition, the RstA regulator activates the expression of this gene. Physiologically, we observed that RcsB-dependent repression is required for the survival of bacteria when they are exposed to pancreatic fluids. We hypothesized that STM1485 plays an important role in Salmonella adaptation to pH changes, during transition in the gastrointestinal tract. We suggest that bacteria surviving the gastrointestinal environment invade the epithelial cells, where they can remain in vacuoles. In this new environment, acidity and magnesium starvation activate the expression of the RstA regulator in a PhoPQ-dependent manner, which in turn induces STM1485 expression. These levels of STM1485 allow increased bacterial replication within vacuoles to continue the course of infection.

细菌通过两组分调节系统调节基因转录，从而生存下来并对环境中的不利变化做出反应。在沙门氏菌鼠伤寒STM1485基因表达是在上皮宿主细胞内复制过程中在低pH值（4.5）下诱导的，但它不参与感测或抵抗这种情况。由于RcsCDB系统在酸性条件下被激活，因此我们研究了该系统是否能够调节STM1485表达。我们证明了酸诱导的RcsB激活通过直接结合启动子来抑制STM1485转录。在相同条件下，RstA调节剂激活该基因的表达。在生理上，我们观察到当细菌暴露于胰液时，RcsB依赖性抑制是细菌生存所必需的。我们假设STM1485在沙门氏菌中起重要作用在胃肠道过渡过程中适应pH值变化。我们建议生存在胃肠环境中的细菌侵入上皮细胞，在那里它们可以留在液泡中。在这种新环境中，酸度和镁饥饿会以PhoPQ依赖的方式激活RstA调节剂的表达，进而诱导STM1485表达。STM1485的这些水平允许液泡内细菌复制增加，从而继续感染过程。