ArticleNature communications2024
Inter-cell type interactions that control JNK signaling in the Drosophila intestine.
Article in Nature communications, 2024. 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.
- The JNK2-microbiome axis modulates gut barrier integrity through microbial acetate.Gut microbes · 2026Article
- Function ofInsects · 2026Article
- Toll signaling controls stem cell proliferation in intestinal regeneration and tumorigenesis.EMBO reports · 2026Article
- Apoptosis-resistant cells drive compensatory proliferation via cell-autonomous and non-autonomous functions of the initiator caspase Dronc.Nature communications · 2025Article
- Activation of a Src-JNK pathway in unscheduled endocycling cells of the Drosophila wing disc induces a chronic wounding response.Genetics · 2025Article
- Temporal and spatial profiling of Aedes albopictus immune responses to chikungunya virus infection.PLoS neglected tropical diseases · 2025Article
- Glycolytic disruption restricts Drosophila melanogaster larval growth via the cytokine Upd3.PLoS genetics · 2025Article
- Cell-death induced immune response and coagulopathy promote cachexia inbioRxiv : the preprint server for biology · 2025Article
- Drosophila Intestine as a Model to Study Tumors.Advances in experimental medicine and biology · 2025Review
- c-Jun N-terminal kinase signaling in aging.Frontiers in aging neuroscience · 2024Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
JNK signaling is a critical regulator of inflammation and regeneration, but how it is controlled in specific tissue contexts remains unclear. Here we show that, in the Drosophila intestine, the TNF-type ligand, Eiger (Egr), is expressed exclusively by intestinal stem cells (ISCs) and enteroblasts (EBs), where it is induced by stress and during aging. Egr preferentially activates JNK signaling in a paracrine fashion in differentiated enterocytes (ECs) via its receptor, Grindelwald (Grnd). N-glycosylation genes (Alg3, Alg9) restrain this activation, and stress-induced downregulation of Alg3 and Alg9 correlates with JNK activation, suggesting a regulatory switch. JNK activity in ECs induces expression of the intermembrane protease Rhomboid (Rho), driving secretion of EGFR ligands Keren (Krn) and Spitz (Spi), which in turn activate EGFR signaling in progenitor cells (ISCs and EBs) to stimulate their growth and division, as well as to produce more Egr. This study uncovers an N-glycosylation-controlled, paracrine JNK-EGFR-JNK feedforward loop that sustains ISC proliferation during stress-induced gut regeneration.
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Registered trials
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