ArticleScience advances2023
The Drosophila tumor necrosis factor receptor, Wengen, couples energy expenditure with gut immunity.
Article in Science advances, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Cross-species TNF-α signaling in mosquitoes promotes malaria transmission.EMBO reports · 2026Article
- Interplay of EGFR, JNK, and ROS signaling in soma-germline communication in the Drosophila testis.Stem cell reports · 2025Article
- Pathogen-induced damage in Drosophila: Uncoupling disease tolerance from resistance.PLoS pathogens · 2025Article
- TNF signaling mediates cellular immune function and promotes malaria parasite killing in the mosquito Anopheles gambiae.PLoS pathogens · 2025Article
- The flux of energy in critical illness and the obesity paradox.Physiological reviews · 2025Review
- Adipocyte-DerivedBiomolecules · 2025Article
- Glial-derived TNF/Eiger signaling promotes somatosensory neurite sculpting.Cellular and molecular life sciences : CMLS · 2025Article
- Reactive oxygen species activate the Drosophila TNF receptor Wengen for damage-induced regeneration.The EMBO journal · 2024Article
- Wengen's hidden powers: ROS triggers a TNFR-dependent tissue regenerative pathway in Drosophila.The EMBO journal · 2024Article
- Inter-cell type interactions that control JNK signaling in the Drosophila intestine.Nature communications · 2024Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is well established that tumor necrosis factor (TNF) plays an instrumental role in orchestrating the metabolic disorders associated with late stages of cancers. However, it is not clear whether TNF/TNF receptor (TNFR) signaling controls energy homeostasis in healthy individuals. Here, we show that the highly conserved Drosophila TNFR, Wengen (Wgn), is required in the enterocytes (ECs) of the adult gut to restrict lipid catabolism, suppress immune activity, and maintain tissue homeostasis. Wgn limits autophagy-dependent lipolysis by restricting cytoplasmic levels of the TNFR effector, TNFR-associated factor 3 (dTRAF3), while it suppresses immune processes through inhibition of the dTAK1/TAK1-Relish/NF-κB pathway in a dTRAF2-dependent manner. Knocking down dTRAF3 or overexpressing dTRAF2 is sufficient to suppress infection-induced lipid depletion and immune activation, respectively, showing that Wgn/TNFR functions as an intersection between metabolism and immunity allowing pathogen-induced metabolic reprogramming to fuel the energetically costly task of combatting an infection.
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