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 neighbors. 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 favorable interaction between V. cholerae and an arthropod host by reducing the nutritional burden of intestinal colonization.
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