Abstract
ABSTRACTFlagellum-driven motility of Salmonella enterica serovar Typhimurium facilitates host colonization. However, the large extracellular flagellum is also a prime target for the immune system. As consequence, expression of flagella is bistable within a population of Salmonella, resulting in flagellated and nonflagellated subpopulations. This allows the bacteria to maximize fitness in hostile environments. The degenerate EAL domain protein RflP (formerly YdiV) is responsible for the bistable expression of flagella by directing the flagellar master regulatory complex FlhD4C2 with respect to proteolytic degradation. Information concerning the environmental cues controlling expression of rflP and thus about the bistable flagellar biosynthesis remains ambiguous. Here, we demonstrated that RflP responds to cell envelope stress and alterations of outer membrane integrity. Lipopolysaccharide (LPS) truncation mutants of Salmonella Typhimurium exhibited increasing motility defects due to downregulation of flagellar gene expression. Transposon mutagenesis and genetic profiling revealed that σ24 (RpoE) and Rcs phosphorelay-dependent cell envelope stress response systems sense modifications of the lipopolysaccaride, low pH, and activity of the complement system. This subsequently results in activation of RflP expression and degradation of FlhD4C2 via ClpXP. We speculate that the presence of diverse hostile environments inside the host might result in cell envelope damage and would thus trigger the repression of resource-costly and immunogenic flagellum biosynthesis via activation of the cell envelope stress response.
Highlights
Flagellum-driven motility of Salmonella enterica serovar Typhimurium facilitates host colonization
The enteropathogen Salmonella enterica serovar Typhimurium is able to move in a directed manner using flagellum-mediated propulsion in a process known as chemotaxis [1]
Of de novo protein synthesis and found that the FlhC protein was degraded substantially faster in the ΔrfaG LPS truncation mutant than in the Wt strain (Fig. 2C). These results show that the reduced motility of the LPS truncation mutants was due to posttranscriptional regulation at the level of the flagellar master regulatory complex, FlhD4C2
Summary
Flagellum-driven motility of Salmonella enterica serovar Typhimurium facilitates host colonization. The degenerate EAL domain protein RflP (formerly YdiV) is responsible for the bistable expression of flagella by directing the flagellar master regulatory complex FlhD4C2 with respect to proteolytic degradation. Transposon mutagenesis and genetic profiling revealed that 24 (RpoE) and Rcs phosphorelay-dependent cell envelope stress response systems sense modifications of the lipopolysaccaride, low pH, and activity of the complement system This subsequently results in activation of RflP expression and degradation of FlhD4C2 via ClpXP. We speculate that downregulation of flagellum synthesis after cell envelope damage in hostile environments aids survival of Salmonella during late stages of infection and provides a means to escape recognition by the immune system. Typhimurium appears to exploit the above-mentioned heterogeneous regulation of flagellum production during the early stages of infection in addition to population-wide repression of flagellar gene expression during systemic infection. Knowledge concerning the signals controlling the expression of the bistable switch protein RflP remained elusive
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