[ODP-090] Xenogeneic silencing-mediated regulation of T3SS2 in Vibrio parahaemolyticus
A marine bacterium Vibrio parahaemolyticus is a common seafood-borne pathogen that causes acute diarrhea in humans. A major virulence determinant of V. parahaemolyticus is a type III secretion system 2 (T3SS2) encoded on a pathogenicity island, Vp-PAI. The T3SS2 gene expression is affected by external environmental cues such as temperature and osmolarity; however, the underlying mechanism remains elusive. Here, we show that histone-like nucleoid-structuring protein (H-NS), a xenogeneic silencing protein, regulates T3SS2 gene expression through transcriptional repression of a virulence regulator VtrB. VtrB production was repressed at non-permissive conditions while production of its upstream regulator VtrA was consistent, and this repression was broken by the deletion of hns. We found that H-NS binding sites partially overlap VtrA binding site within the vtrB promoter, which may block transcriptional activation of vtrB. H-NS suppress its target genes by binding and multimerization to form filaments and/or bridges nucleoprotein complex. Mutations at dimerization domain of H-NS abolished repression of VtrB production in vivo but retains its binding ability to the vtrB promoter in vitro, suggesting that H-NS multimerization is important for VtrB repression. Together, these findings demonstrate that H-NS plays a pivotal role in T3SS2 genes expression in V. parahaemolyticus.