The Vibrio cholerae quorum sensing master regulator HapR represses virulence factor expression and biofilm formation at high cell density. In this manuscript, we show that V. cholerae quorum sensing decreases pathogen virulence in the model arthropod, Drosophila melanogaster. We show that this decrease in virulence can be attributed to repression of succinate uptake by HapR. Infection with a HapR mutant results in depletion of host lipid stores and host death. Dietary supplementation with succinate allows the host to retain its lipid stores, thus prolonging survival.
Mammalian and arthropod hosts depend on the metabolic signals generated by intestinal bacteria to maintain homeostasis. While pathogens can disrupt homeostasis by consuming these metabolic signals, our study reveals a novel role for V. cholerae quorum sensing in repressing bacterial consumption of succinate to ensure nutritional cooperation of this pathogen with its arthropod host.