multiformis: Nmul; Polaromonas: Pola. 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. “
“Vibrio cholerae colonizes the human intestine and causes the acute diarrheal disease cholera. Flagellar-mediated

chemotaxis contributes to intestinal colonization as well as infectivity. The virulence-regulatory protein ToxT activates transcription of the genes encoding the major virulence factors cholera toxin and toxin coregulated pilus. ToxT additionally activates transcription of two genes, tcpI and acfB, located within the Vibrio Pathogenicity Island predicted to encode methyl-accepting chemoreceptors. see more We show that disruption of either tcpI or acfB individually does not noticeably affect V. cholerae intestinal colonization within the infant mouse, but disruption of both tcpI and acfB leads to a decrease in intestinal colonization. These results suggest that TcpI and AcfB may have overlapping or redundant chemotactic functions that contribute to V. cholerae intestinal buy SP600125 colonization. Vibrio cholerae causes the acute diarrheal disease cholera in humans. The bacteria are acquired by the ingestion of contaminated water or food, and colonize the intestine. Vibrio cholerae expresses virulence factors

within the intestinal tract that lead to disease symptoms, most notably the cholera toxin (CT), which is responsible for the acute Cyclin-dependent kinase 3 watery diarrhea characteristic of cholera (Holmgren & Svennerholm, 1989). The organisms also express the toxin coregulated

pilus (TCP), a Type IV pilus that is required for intestinal colonization (Taylor et al., 1987). A regulatory cascade commonly referred to as the ToxR regulon coordinately regulates the expression of CT and TCP in response to environmental signals within the host (for a review, see Childers & Klose, 2007). Activation of the ToxR regulon culminates in the expression of the regulatory protein ToxT, which then directly activates transcription of the genes encoding CT and TCP (DiRita et al., 1991). The toxT and tcp genes lie within a cluster of horizontally acquired virulence genes in the Vibrio Pathogenicity Island (VPI) (Karaolis et al., 1998), while the ctx genes are within the lysogenic bacteriophage CTXφ (Waldor & Mekalanos, 1996). Bacterial chemotaxis is accomplished by a number of proteins that constitute a signaling cascade. Methyl-accepting chemoreceptors (MCP) are membrane-spanning proteins that undergo a conformational change upon binding a chemoattractant or a repellant, and this stimulates a signaling cascade that ultimately results in the formation of a phosphorylated chemotaxis protein CheY that interacts with the flagellum and switches the rotation from counterclockwise to clockwise (for a review, see Baker et al., 2006).