Document type

Article

Version

Published version

Publication date

Publication license

cc-by (c)  Esteban-Collado, José. et al., 2024
Please use this identifier to cite or link to this item: https://hdl.handle.net/2445/221858

Reactive oxygen species activate the Drosophila TNF receptor Wengen for damage-induced regeneration

Journal Title

Director/Tutor

Journal ISSN

Volume Title

Abstract

Tumor necrosis factor receptors (TNFRs) control pleiotropic pro-inflammatory functions that range from apoptosis to cell survival. The ability to trigger a particular function will depend on the upstream cues, association with regulatory complexes, and downstream pathways. In Drosophila melanogaster, two TNFRs have been identified, Wengen (Wgn) and Grindelwald (Grnd). Although several reports associate these receptors with JNK-dependent apoptosis, it has recently been found that Wgn activates a variety of other functions. We demonstrate that Wgn is required for survival by protecting cells from apoptosis. This is mediated by dTRAF1 and results in the activation of p38 MAP kinase. Remarkably, Wgn is required for apoptosis-induced regeneration and is activated by the reactive oxygen species (ROS) produced following apoptosis. This ROS activation is exclusive for Wgn, but not for Grnd, and can occur after knocking down Eiger/TNFα. The extracellular cysteine-rich domain of Grnd is much more divergent than that of Wgn, which is more similar to TNFRs from other animals, including humans. Our results show a novel TNFR function that responds to stressors by ensuring p38-dependent regeneration.

Citation

Citation

ESTEBAN-COLLADO, José, et al. Reactive oxygen species activate the Drosophila TNF receptor Wengen for damage-induced regeneration. The EMBO Journal. 2024. Vol. 43, num. 17, pags. 3604-3626. ISSN 0261-4189. [consulted: 17 of June of 2026]. Available at: https://hdl.handle.net/2445/221858

Export metadata

JSON - METS

Share record