In the enteric pathogen Salmonella enterica serovar Typhimurium, invasion and motility are coordinated by the master regulator HilD, which induces expression of the type III secretion system 1 (T3SS1) and motility genes. Methyl-accepting chemotaxis proteins (MCPs) detect specific ligands and control the direction of the flagellar motor, promoting tumbling and changes in direction (if a repellent is detected) or smooth swimming (in the presence of an attractant). Here, we show that HilD induces smooth swimming by upregulating an uncharacterized MCP (McpC), and this is important for invasion of epithelial cells. Remarkably, in vitro assays show that McpC can suppress tumbling and increase smooth swimming in the absence of exogenous ligands. Expression of mcpC is repressed by the universal regulator H-NS, which can be displaced by HilD. Our results highlight the importance of smooth swimming for Salmonella Typhimurium invasiveness and indicate that McpC can act via a ligand-independent mechanism when incorporated into the chemotactic receptor array.

在肠道病原体鼠伤寒沙门氏菌中，侵袭和运动由主调节因子 HilD 协调，HilD 诱导 III 型分泌系统 1 (T3SS1) 和运动基因的表达。甲基接受趋化蛋白 (MCP) 检测特定配体并控制鞭毛运动的方向，促进翻滚和方向改变（如果检测到驱虫剂）或平稳游泳（在存在引诱剂的情况下）。在这里，我们发现 HilD 通过上调未表征的 MCP (McpC) 来诱导平滑游泳，这对于上皮细胞的侵袭很重要。值得注意的是，体外试验表明，在没有外源配体的情况下，McpC 可以抑制翻滚并增加平滑游泳。 mcpC的表达受到通用调节因子 H-NS 的抑制，而 H-NS 可以被 HilD 取代。我们的结果强调了平滑游动对于鼠伤寒沙门氏菌侵袭性的重要性，并表明当纳入趋化受体阵列时，McpC 可以通过配体独立机制发挥作用。