ArticlePLoS genetics2016
Remote Control of Intestinal Stem Cell Activity by Haemocytes in Drosophila.
Article in PLoS genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.
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Who cites it
85 citing papers in PubMed, 151 citations in OpenAlex.
- Macrophage restriction inScience advances · 2026Article
- Damage recognition by intestinal stem cells via Draper promotes adult Drosophila midgut regeneration.The EMBO journal · 2026Article
- Heme acts as a metabolic brake on erebosis in the Drosophila gut.PLoS biology · 2026Article
- Gut-derived Unpaired-3 cytokine signaling promotes systemic hypoxia tolerance in Drosophila.Disease models & mechanisms · 2026Article
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- Chronic intestinal immune activation reveals separable impacts of inflammation and barrier loss on hallmarks of ageing.PloS one · 2026Article
- Insect immune systems: same same but different but still same.Frontiers in immunology · 2026Review
- An updated proteomic analysis ofFly · 2025Article
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- Mosquito immune cells enhance dengue and Zika virus infection in Aedes aegypti.Nature communications · 2025Article
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- Anopheles gambiae phagocytic hemocytes promote Plasmodium falciparum infection by regulating midgut epithelial integrity.Nature communications · 2025Article
- Host-Microbe Interactions in Drosophila Cancer.Advances in experimental medicine and biology · 2025Review
- Remote disruption of intestinal homeostasis by Mycobacterium abscessus is detrimental to Drosophila survival.Scientific reports · 2024Article
- Sex-dimorphic tumor growth is regulated by tumor microenvironmental and systemic signals.Science advances · 2024Article
- Review
- DNA damage signaling ineLife · 2024Article
- Drosophila activins adapt gut size to food intake and promote regenerative growth.Nature communications · 2024Article
- Review
- Professional phagocytes are recruited for the clearance of obsolete nonprofessional phagocytes in theFrontiers in immunology · 2024Article
25 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The JAK/STAT pathway is a key signaling pathway in the regulation of development and immunity in metazoans. In contrast to the multiple combinatorial JAK/STAT pathways in mammals, only one canonical JAK/STAT pathway exists in Drosophila. It is activated by three secreted proteins of the Unpaired family (Upd): Upd1, Upd2 and Upd3. Although many studies have established a link between JAK/STAT activation and tissue damage, the mode of activation and the precise function of this pathway in the Drosophila systemic immune response remain unclear. In this study, we used mutations in upd2 and upd3 to investigate the role of the JAK/STAT pathway in the systemic immune response. Our study shows that haemocytes express the three upd genes and that injury markedly induces the expression of upd3 by the JNK pathway in haemocytes, which in turn activates the JAK/STAT pathway in the fat body and the gut. Surprisingly, release of Upd3 from haemocytes upon injury can remotely stimulate stem cell proliferation and the expression of Drosomycin-like genes in the intestine. Our results also suggest that a certain level of intestinal epithelium renewal is required for optimal survival to septic injury. While haemocyte-derived Upd promotes intestinal stem cell activation and survival upon septic injury, haemocytes are dispensable for epithelium renewal upon oral bacterial infection. Our study also indicates that intestinal epithelium renewal is sensitive to insults from both the lumen and the haemocoel. It also reveals that release of Upds by haemocytes coordinates the wound-healing program in multiple tissues, including the gut, an organ whose integrity is critical to fly survival.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.