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Reactive oxygen species activate the Drosophila TNF receptor Wengen for damage-induced regeneration.
The EMBO Journal ( IF 9.4 ) Pub Date : 2024-07-17 , DOI: 10.1038/s44318-024-00155-9
José Esteban-Collado 1, 2 , Mar Fernández-Mañas 1, 3 , Manuel Fernández-Moreno 1, 4, 5 , Ignacio Maeso 1, 4 , Montserrat Corominas 1, 2 , Florenci Serras 1, 2
Affiliation  

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.

中文翻译:


活性氧物质激活果蝇 TNF 受体 Wengen,以实现损伤诱导的再生。



肿瘤坏死因子受体 (TNFR) 控制从细胞凋亡到细胞存活的多效性促炎症功能。触发特定功能的能力将取决于上游线索、与调节复合物的关联以及下游途径。在果蝇中,已鉴定出两种 TNFR:Wengen (Wgn) 和 Grindelwald (Grnd)。尽管一些报告将这些受体与 JNK 依赖性细胞凋亡联系起来,但最近发现 Wgn 可以激活多种其他功能。我们证明 Wgn 是通过保护细胞免于凋亡来维持生存所必需的。这是由 dTRAF1 介导的,并导致 p38 MAP 激酶激活。值得注意的是,Wgn 是细胞凋亡诱导的再生所必需的,并且由细胞凋亡后产生的活性氧 (ROS) 激活。这种 ROS 激活是 Wgn 独有的,但 Grnd 则不然,并且可以在击倒 Eiger/TNFα 后发生。 Grnd 的胞外富含半胱氨酸结构域比 Wgn 的差异更大,后者与其他动物(包括人类)的 TNFR 更相似。我们的结果显示了一种新的 TNFR 功能,可通过确保 p38 依赖性再生来响应应激源。
更新日期:2024-07-17
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