Mutation of the cognate response regulator gene rcsB restored full virulence to the rcsC constitutive mutant , indicating that virulence attenuation results from aberrant expression of RcsB-regulated genes.The virulence attenuation phenotype was partially dependent on the regulatory gene rcsA , which is necessary for transcription of certain RcsB-regulated genes , and on the RcsB-and RcsA-dependent colanic acid capsule synthesis cps operon .
Both an rcsB single mutant and an rcsC11 rcsB double mutant exhibited wild-type virulence ( Table 1 ; Fig. 1 ) , indicating that the attenuated phenotype of the rcsC11 mutant is entirely dependent on RcsB-regulated genes and ruling out cross-talk of the mutant RcsC11 protein to other two-component systems as responsible for attenuation .
of the RcsC/YojN/RcsB regulatory system due to the rcsC11 allele in the sensor RcsC renders Salmonella avirulent , and that inactivation of the response regulator gene rcsB restores full virulence to the rcsC11 mutant , indicative that its attenuated phenotype results from aberrant expression of RcsB-regulated genes .
We did not observe a decrease in Δ in a wza yjb rcsB mutant beyond what is observed in the rcsB mutant , suggesting that no additional RcsB-regulated factors are required for PMF maintenance ( see Fig .