Microbiota reduce Drosophila triacylglyceride density by providing pantothenate
Metabolism follows ground-rules that evolved in ancient bacteria: as a legacy, animal gut microbiota have abundant opportunity to modulate host metabolism, via conserved mechanisms. When these effects are beneficial, natural selection should favour hosts that reciprocally support bacterial growth. Whether microbes simply nourish hosts or more profoundly reprogram host metabolism remains to be established. Here we show that Acetobacter promote Drosophila coenzyme A, an ancient signalling metabolite, reprogramming host metabolism and generating a state that reciprocally supports bacterial growth. Impairing pathways from bacterial pantothenate to host coenzyme A increases host lipid storage, reduces nitrogen excretion, and diminishes bacterial load. These processes correspond to reprogrammed host carbohydrate handling and tissue-specific acyl-CoA pools, but live bacteria and short-chain fatty acids are dispensable. These results outline a simple microbial basis for complex host metabolic effects, via mechanisms that precede the origins of metazoa, facilitating metabolic and symbiotic homeostasis.