ArticleDisease models & mechanisms2022
TOR signalling is required for host lipid metabolic remodelling and survival following enteric infection in Drosophila.
Article in Disease models & mechanisms, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 12 citations in OpenAlex.
- Citrus aurantium honey-mediated gut homeostasis and anti-inflammation via Thorl/Nprl2-TORC1 signaling: Network pharmacology and Drosophila validation.Animal models and experimental medicine · 2026Article
- Evolution, multifunctionality, and agricultural potential of insect microbiomes and the holobiont concept.The ISME journal · 2026Review
- BMP-dependent mobilization of fatty acid metabolism promotes Caenorhabditis elegans survival on a bacterial pathogen.Disease models & mechanisms · 2025Article
- Supporting the evolution of infectious disease research.Disease models & mechanisms · 2024Article
- Supporting the evolution of infectious disease research.Disease models & mechanisms · 2024Article
- Interactions between innate immunity and insulin signaling affect resistance to infection in insects.Frontiers in immunology · 2023Review
- TGF-β pathways in aging and immunity: lessons fromFrontiers in genetics · 2023Review
- Enteric bacterial infection in Drosophila induces whole-body alterations in metabolic gene expression independently of the immune deficiency signaling pathway.G3 (Bethesda, Md.) · 2022Article
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4 authors at 1 institution in 1 country.
Funding
Abstract
When infected by enteric pathogenic bacteria, animals need to initiate local and whole-body defence strategies. Although most attention has focused on the role of innate immune anti-bacterial responses, less is known about how changes in host metabolism contribute to host defence. Using Drosophila as a model system, we identify induction of intestinal target-of-rapamycin (TOR) kinase signalling as a key adaptive metabolic response to enteric infection. We find that enteric infection induces both local and systemic induction of TOR independently of the Immune deficiency (IMD) innate immune pathway, and we see that TOR functions together with IMD signalling to promote infection survival. These protective effects of TOR signalling are associated with remodelling of host lipid metabolism. Thus, we see that TOR is required to limit excessive infection-mediated wasting of host lipid stores by promoting an increase in the levels of gut- and fat body-expressed lipid synthesis genes. Our data support a model in which induction of TOR represents a host tolerance response to counteract infection-mediated lipid wasting in order to promote survival. This article has an associated First Person interview with the first author of the paper.
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