Figure 3.

Examples of virulence gene regulation by the Rcs ESR. The Rcs system is induced by various signals deleterious to the outer membrane such as osmotic shock, desiccation, and overproduction of envelope proteins. Detection of some signals involves accessory proteins such as RcsF and others not shown. All signals converge of the IM histidine kinase RcsC, which transfers phosphate (P) to the cytoplasmic response regulator RcsB via the intermediary IM protein RcsD. RcsB can regulate target promoters as a homodimer or as a heterodimer with RcsA, or with the RcsA homologues RmpA and RmpA2 that are found in hypermucoviscous (HMV) strains of K. pneumoniae. Positively controlled target promoters include galF in encapsulated E. coli K strains, which increases precursors available for Group I capsule production. Similarly, ugd is an activated target in Salmonella, which is needed to make a precursor for LPS modification that increases CAMP resistance. In Y. enterocolitica (Y. ent) RcsB is involved in activation of the major operon encoding regulatory and structural components of the Ysa T3SS, but it is not known if this regulation is direct. Very recent data from Y. pseudotuberculosis (Y. ptb) has also shown that RcsB activates genes encoding the Ysc T3SS via direct induction of the lcrF gene, encoding the master Ysc T3SS regulator (see text). In Salmonella, RcsB drives the production of an antisense transcript encompassing the distal end of the fliLMNOPQR operon, which is involved in downregulating multiple virulence genes including those encoding components of the SPI-1 and SPI-2 T3SS systems. In HMV K. pneumoniae, RcsB, most likely as a heterodimer with RmpA or RmpA2, activates the cps operon responsible for capsular polysaccharide production.