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The virulence regulator ToxR initiates and coordinates gene expression needed by  Vibrio cholerae  to colonize the small intestine and cause disease. Despite its prominence in  V .  cholerae  virulence, our understanding of the direct ToxR regulon is limited to four genes:  toxT ,  ompT ,  ompU  and  ctxA . Here, we determine ToxR’s genome-wide DNA-binding profile and demonstrate that ToxR is a global regulator of both progenitor genome-encoded genes and horizontally acquired islands that encode  V .  cholerae’ s major virulence factors and define pandemic lineages. We show that ToxR shares more than a third of its regulon with the histone-like nucleoid structuring protein H-NS, and antagonizes H-NS binding at shared binding locations. Importantly, we demonstrate that this regulatory interaction is the critical function of ToxR in  V .  cholerae  colonization and biofilm formation. In the absence of H-NS, ToxR is no longer required for  V .  cholerae  to colonize the infant mouse intestine or for robust biofilm formation. We further illustrate a dramatic difference in regulatory scope between ToxR and other prominent virulence regulators, despite similar predicted requirements for DNA binding. Our results suggest that factors in addition to primary DNA structure influence the ability of ToxR to recognize its target promoters.

ToxR Antagonizes H-NS Regulation of Horizontally Acquired Genes to Drive Host Colonization