Fast enterocyte regrowth after infection involves a reverse metabolic flux driven by an amino acid transporter.

Upon exposure to a bacterial pore-forming toxin, enterocytes rapidly purge their apical cytoplasm into the gut lumen, resulting in a thin intestinal epithelium. The enterocytes regain their original shape and thickness within 16 h after the ingestion of the bacteria. Here, we show that the regrowth of enterocytes entails an inversion of metabolic fluxes from the organism back toward the intestine.

Drosophila melanogaster establishes a species-specific mutualistic interaction with stable gut-colonizing bacteria.

Animals live together with diverse bacteria that can impact their biology. In Drosophila melanogaster, gut-associated bacterial communities are relatively simple in composition but also have a strong impact on host development and physiology. It is generally assumed that gut bacteria in D.

The Toll-dorsal pathway is required for resistance to viral oral infection in Drosophila.

Pathogen entry route can have a strong impact on the result of microbial infections in different hosts, including insects. Drosophila melanogaster has been a successful model system to study the immune response to systemic viral infection. Here we investigate the role of the Toll pathway in resistance to oral viral infection in D.