Abstract
While much has been learned regarding the genetic basis of host-pathogen interactions, less is known about the molecular basis of a pathogen's survival in the environment. Biofilm formation on abiotic surfaces represents a survival strategy utilized by many microbes. Here it is shown that Vibrio cholerae El Tor does not use the virulence-associated toxin-coregulated pilus to form biofilms on borosilicate but rather uses the mannose-sensitive hemagglutinin (MSHA) pilus, which plays no role in pathogenicity. In contrast, attachment of V. cholerae to chitin is shown to be independent of the MSHA pilus, suggesting divergent pathways for biofilm formation on nutritive and nonnutritive abiotic surfaces.
Publication types
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Comparative Study
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Bacterial Adhesion
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Bacterial Proteins / genetics
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Bacterial Proteins / metabolism
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Bacterial Proteins / physiology*
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Biofilms / growth & development*
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Boron Compounds / metabolism
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Cellulose / metabolism
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Chitin / metabolism
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Fimbriae Proteins*
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Fimbriae, Bacterial / genetics
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Fimbriae, Bacterial / physiology*
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Hemagglutinins / genetics
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Hemagglutinins / metabolism
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Hemagglutinins / physiology*
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Mannose / metabolism*
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Mannose-Binding Lectin
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Mutation
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Silicates / metabolism
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Toxins, Biological / metabolism
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Vibrio cholerae / metabolism
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Vibrio cholerae / pathogenicity
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Vibrio cholerae / physiology*
Substances
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Bacterial Proteins
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Boron Compounds
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Hemagglutinins
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Mannose-Binding Lectin
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MshA protein, Vibrio cholerae
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Silicates
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Toxins, Biological
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Chitin
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Fimbriae Proteins
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Cellulose
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Mannose