The Rcs signal transduction pathway is triggered by ECA structure alterations in Serratia marcescens

CASTELLI, MARÍA EUGENIA; GARCIA VESCOVI ELEONORA

Puerto Madryn

Congreso; XLVI Reunión Anual- Sociedad Argentina de investigación en Bioquímica y Biología Molecular; 2010

SAIB

S. marcescens is a gram negative enteric bacterium that acts as an opportunistic pathogen. Despite numerous reported S. marcescens infections and the emergence of antibiotic-resistant strains, the virulence mechanisms of this organism are unresolved. The enterobacterial common antigen is a highly conserved exopolysaccharide in enteric bacteria which role remains uncharacterized. Previously, we have demonstrated that disrupting the integrity of the ECA biosynthetic pathway imposed severe deficiencies to S. marcescens motile capacity. We show that alterations in the ECA structure activate the Rcs phosphorelay, which results in the repression of the flagellar regulatory cascade. In addition, a detailed analysis of wec cluster mutant strains, that provoke the disruption of the ECA biosynthesis at different levels, suggests that the absence of the periplasmic ECA cyclic structure could be the signal detected by the RcsF-RcsCDB phosphorelay. We also identify SMA1167 as a member of the Rcs regulon, and show that high osmolarity induces Rcs activity in this bacterium. These results widen the knowledge about the identity of envelope stress signals that induce the Rcs regulatory system. They also provide a new perspective to understand the phylogenetic conservation of ECA among enterobacteria and the basis for virulence attenuation detected in wec mutant strains in other pathogenic bacteria.