ArticlePLoS genetics2015
ROS-Induced JNK and p38 Signaling Is Required for Unpaired Cytokine Activation during Drosophila Regeneration.
Article in PLoS genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 154 papers.
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Who cites it
154 citing papers in PubMed.
- 3D genome organization in tissue regeneration involves long-range chromatin loops.Science advances · 2026Article
- AlteredeNeuro · 2026Article
- Epithelial cell extrusion underlies starvation-induced cell loss in a sea anemone.Nature communications · 2026Article
- Reactive oxygen species drive wound epithelium and blastema formation in regenerating tail of Scincella tsinlingensis.Frontiers in zoology · 2026Article
- Draper-mediated efferocytosis bybioRxiv : the preprint server for biology · 2026Article
- Wdr4 regulates ribosome biogenesis and intestinal homeostasis via let-7.EMBO reports · 2026Article
- Article
- Duox-driven ROS release by glia promotes regeneration in the adult Drosophila brain.EMBO reports · 2026Article
- Sex-dependent plasticity of adult neural tissue in response to damage.Development (Cambridge, England) · 2026Article
- CircRNA-encoded protein fine-tunes ROS homeostasis and engages conserved JAK-STAT antiviral defenses inJournal of virology · 2026Article
- Niche-derived exosomes controlFrontiers in immunology · 2026Article
- The homeodomain-interacting protein kinase Hipk promotes apoptosis by stabilizing the active form of Dronc.Cell death discovery · 2025Article
- Myc and Tor drive growth and cell competition in the regeneration blastema of Drosophila wing imaginal discs.Development (Cambridge, England) · 2025Article
- A JAK/STAT-Pdk1-S6K axis bypasses systemic growth restrictions to promote regeneration.Nature communications · 2025Article
- Interplay of EGFR, JNK, and ROS signaling in soma-germline communication in the Drosophila testis.Stem cell reports · 2025Article
- Cell Death, Compensatory Proliferation, and Cell Competition.Annual review of genetics · 2025Review
- A threshold level of JNK activates damage-responsive enhancers via JAK/STAT to promote tissue regeneration.Development (Cambridge, England) · 2025Article
- Myc and Tor drive growth and cell competition in the regeneration blastema ofbioRxiv : the preprint server for biology · 2025Article
- Glycolytic disruption restricts Drosophila melanogaster larval growth via the cytokine Upd3.PLoS genetics · 2025Article
- Epithelial cell competition is promoted by signaling from immune cells.Nature communications · 2025Article
94 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Upon apoptotic stimuli, epithelial cells compensate the gaps left by dead cells by activating proliferation. This has led to the proposal that dying cells signal to surrounding living cells to maintain homeostasis. Although the nature of these signals is not clear, reactive oxygen species (ROS) could act as a signaling mechanism as they can trigger pro-inflammatory responses to protect epithelia from environmental insults. Whether ROS emerge from dead cells and what is the genetic response triggered by ROS is pivotal to understand regeneration of Drosophila imaginal discs. We genetically induced cell death in wing imaginal discs, monitored the production of ROS and analyzed the signals required for repair. We found that cell death generates a burst of ROS that propagate to the nearby surviving cells. Propagated ROS activate p38 and induce tolerable levels of JNK. The activation of JNK and p38 results in the expression of the cytokines Unpaired (Upd), which triggers the JAK/STAT signaling pathway required for regeneration. Our findings demonstrate that this ROS/JNK/p38/Upd stress responsive module restores tissue homeostasis. This module is not only activated after cell death induction but also after physical damage and reveals one of the earliest responses for imaginal disc regeneration.
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