Abstract
Vibrio cholerae colonizes the human terminal ileum to cause cholera, and the arthropod intestine and exoskeleton to persist in the aquatic environment. Attachment to these surfaces is regulated by the bacterial quorum-sensing signal transduction cascade, which allows bacteria to assess the density of microbial neighbours. Intestinal colonization with V. cholerae results in expenditure of host lipid stores in the model arthropod Drosophila melanogaster. Here we report that activation of quorum sensing in the Drosophila intestine retards this process by repressing V. cholerae succinate uptake. Increased host access to intestinal succinate mitigates infection-induced lipid wasting to extend survival of V. cholerae-infected flies. Therefore, quorum sensing promotes a more favourable interaction between V. cholerae and an arthropod host by reducing the nutritional burden of intestinal colonization.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Adipose Tissue
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Animals
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Arthropods / microbiology*
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Bacterial Proteins / genetics
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Bacterial Proteins / metabolism
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Biofilms / growth & development
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Disease Models, Animal
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Drosophila Proteins / genetics
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Drosophila melanogaster / microbiology
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Female
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Gene Expression Profiling
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Gene Expression Regulation, Bacterial
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Gene Knockdown Techniques
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Host-Pathogen Interactions / physiology
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Intestines / microbiology*
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Lipolysis
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Organ Size
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Quorum Sensing / physiology*
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Signal Transduction
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Somatomedins / genetics
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Succinic Acid / metabolism
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Triglycerides / metabolism
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Vibrio cholerae / genetics
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Vibrio cholerae / growth & development
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Vibrio cholerae / metabolism*
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Vibrio cholerae / pathogenicity*
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Virulence / genetics
Substances
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Bacterial Proteins
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Drosophila Proteins
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Ilp6 protein, Drosophila
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Somatomedins
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Triglycerides
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Succinic Acid