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• W1972038449 startingPage "1528" @default.
• W1972038449 abstract "The bacterium Vibrio cholerae , like other human pathogens that reside in environmental reservoirs, survives predation by unicellular eukaryotes. Strains of the O1 and O139 serogroups cause cholera, whereas non-O1/non-O139 strains cause human infections through poorly defined mechanisms. Using Dictyostelium discoideum as a model host, we have identified a virulence mechanism in a non-O1/non-O139 V. cholerae strain that involves extracellular translocation of proteins that lack N-terminal hydrophobic leader sequences. Accordingly, we have named these genes “VAS” genes for virulence-associated secretion, and we propose that these genes encode a prototypic “type VI” secretion system. We show that vas genes are required for cytotoxicity of V. cholerae cells toward Dictyostelium amoebae and mammalian J774 macrophages by a contact-dependent mechanism. A large number of Gram-negative bacterial pathogens carry genes homologous to vas genes and potential effector proteins secreted by this pathway (i.e., hemolysin-coregulated protein and VgrG). Mutations in vas homologs in other bacterial species have been reported to attenuate virulence in animals and cultured macrophages. Thus, the genes encoding the VAS-related, type VI secretion system likely play an important conserved function in microbial pathogenesis and represent an additional class of targets for vaccine and antimicrobial drug-based therapies." @default.
• W1972038449 created "2016-06-24" @default.
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• W1972038449 date "2006-01-23" @default.
• W1972038449 modified "2023-10-14" @default.
• W1972038449 title "Identification of a conserved bacterial protein secretion system in <i>Vibrio cholerae</i> using the <i>Dictyostelium</i> host model system" @default.
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• W1972038449 doi "https://doi.org/10.1073/pnas.0510322103" @default.
• W1972038449 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1345711" @default.
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