Motility revertants of opgGH mutants of Salmonella enterica serovar Typhimurium remain defective in mice virulence.

We recently demonstrated that osmoregulated periplasmic glucans (OPGs) of Salmonella enterica serovar Typhimurium are required for optimal mouse virulence. However, lack of OPGs also generated pleiotropic phenotypes such as reduced motility and slower growth rate under hypoosmotic growth conditions. Whether the observed suboptimal virulence of opg mutants was due to reduced motility was investigated by isolating fully motile revertants of opgGH mutants. Motility revertants remained defective in OPGs synthesis and restitution of motility did not restore mouse virulence. In Escherichia coli, inactivation of rcsB, rcsD, and rcsF lead to restoration of motility in opg mutants, while in Salmonella strains, inactivation of the Rcs pathway is known to attenuate virulence. DNA sequence analysis revealed that except for two silent mutations no other changes in the DNA sequences of Rcs pathway genes were detected in the motility-revertant strain. Moreover, transcripts of all the Rcs phosphorelay pathway genes were detected in opgGH mutants and revertant strain. The data suggest that Salmonella may have distinctive regulatory elements in addition to Rcs phosphorelay genes to rescue motility of opg mutants and affecting also mouse virulence.