ToxT-dependent methyl-accepting chemoreceptors AcfB and TcpI contribute to Vibrio cholerae intestinal colonization

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 c...

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Bibliographic Details
Published in:FEMS microbiology letters 2010, Vol.302 (2), p.99-105
Main Authors: Chaparro, Adriana Paola, Ali, Syed Khalid, Klose, Karl E
Format: Article
Language:English
Subjects:
Animals
Bacterial Proteins - genetics
Bacterial Proteins - physiology
Chemoreceptors
Chemotaxis
Cholera
Cholera toxin
Colonization
Colony Count, Microbial
Diarrhea
Disruption
Flagella
Gastrointestinal Tract - microbiology
Gene Deletion
Genes
Humans
Infectivity
Intestine
Membrane Proteins - genetics
Membrane Proteins - physiology
methyl-accepting chemoreceptor
Mice
Microbiology
Pathogenicity
Pathogens
Repressor Proteins - genetics
Repressor Proteins - physiology
Toxins
Transcription
Transcription Factors - physiology
Vibrio cholerae
Vibrio cholerae - growth & development
Vibrio cholerae - pathogenicity
Virulence
Virulence factors
Waterborne diseases
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Summary: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. 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 colonization.
ISSN:0378-1097
1574-6968
DOI:10.1111/j.1574-6968.2009.01835.x