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Home/Research/Paper Chase/Coordinated regulation of accessory genetic elements produces cyclic di-nucleotides for V. cholerae virulence.
Coordinated regulation of accessory genetic elements produces cyclic di-nucleotides for V. cholerae virulence.
Cell.Apr 13, 2012;149(2):358-70.
Davies BW, Bogard RW, Young TS, Mekalanos JJ.
Department of Microbiology and Immunobiology, Harvard Medical School, Boston, MA 02115, USA.
The function of the Vibrio 7(th) pandemic island-1 (VSP-1) in cholera pathogenesis has remained obscure. Utilizing chromatin immunoprecipitation sequencing and RNA sequencing to map the regulon of the master virulence regulator ToxT, we identify a TCP island-encoded small RNA that reduces the expression of a previously unrecognized VSP-1-encoded transcription factor termed VspR. VspR modulates the expression of several VSP-1 genes including one that encodes a novel class of di-nucleotide cyclase (DncV), which preferentially synthesizes a previously undescribed hybrid cyclic AMP-GMP molecule. We show that DncV is required for efficient intestinal colonization and downregulates V. cholerae chemotaxis, a phenotype previously associated with hyperinfectivity. This pathway couples the actions of previously disparate genomic islands, defines VSP-1 as a pathogenicity island in V. cholerae, and implicates its occurrence in 7(th) pandemic strains as a benefit for host adaptation through the production of a regulatory cyclic di-nucleotide.