Our data on the stress response behavior of a V. choleraeΔphoB mutant suggests that PhoB modulates stress response but differs from the pattern reported for rpoS and ppk mutants (Yildiz & Schoolnik, 1998; Jahid et al., 2006). For instance, global gene expression profiling of an rpoS mutant revealed that RpoS positively affects the expression of the catalase peroxidase PerA (VC1560) and cytochrome c551 peroxidase Venetoclax ic50 VC0089 (Silva et al., 2008). In contrast, deletion of phoB in V. cholerae was found to affect the expression the alkylhydroperoxidase VC0731 (von Kruger et al., 2006) reported to protect against oxidative stress under
conditions of phosphate starvation (Moreau et al., 2001). These results are in agreement with our data, suggesting that RpoS and PhoB activate different stress response mechanisms in V. cholerae. Taken together, our results suggest that under conditions of phosphate limitation, elevated expression of HapR and expression of PhoB act to diminish biofilm formation by diminishing VpsT and VpsR, respectively. In parallel, induction of PhoB under conditions of phosphate limitation modulates stress response in an RpoS-independent manner to provide planktonic cells with resistance mechanisms that could be specifically tailored to the phosphate-deprived environment. The finding selleck screening library that phosphate limitation and expression
of PhoB appears to induce V. cholerae to switch to a planktonic life style poses an intriguing question. The planktonic life style could provide fitness when survival depends on interspecies competition for limiting amounts of soluble phosphate. A model for the integration of cell density and nutritional signals in the regulation of biofilm formation is shown in Fig. 6. According to this model, high cell density, carbon starvation and phosphate limitation promote a planktonic life style by enhancing the expression of the negative factor HapR and PhoB (in the case of phosphate limitation). Interestingly, the opposing effects
of CRP and PhoB on Cobimetinib datasheet VpsR expression suggest that VpsR might function to finely adjust the transition between life styles in response to the carbon–phosphate ratio in the environment. Clearly, more research is required to clarify how the complex interplay between cell density and nutritional signals in the aquatic environment coordinately affect biofilm formation, stress response and the persistence of V. cholerae. The present study was supported by grant GM008248 from the National Institute of General Medical Sciences to A.J.S and PHS grant AI63187 from the National Institute of Allergy and Infectious Disease to J.A.B. Table S1. Strains, plasmids and primers Please note: Wiley-Blackwell is not responsible for the content or functionality of any supporting materials supplied by the authors. Any queries (other than missing material) should be directed to the corresponding author for the article.