ArticleScientific reports2019
JNK-mediated Slit-Robo signaling facilitates epithelial wound repair by extruding dying cells.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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Who cites it
12 citing papers in PubMed, 23 citations in OpenAlex.
- Wound-induced eyespots on butterfly wings at the intersection of immune response and pigmentation development.BMC biology · 2025Article
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- Genetic risk variants implicate impaired maintenance and repair of periodontal tissues as causal for periodontitis-A synthesis of recent findings.Periodontology 2000 · 2025Review
- Reprogramming macrophages with R848-loaded artificial protocells to modulate skin and skeletal wound healing.Journal of cell science · 2024Article
- The Role of SLIT3-ROBO4 Signaling in Endoplasmic Reticulum Stress-Induced Delayed Corneal Epithelial and Nerve Regeneration.Investigative ophthalmology & visual science · 2024Article
- Imaginal Disc Regeneration: Something Old, Something New.Cold Spring Harbor perspectives in biology · 2022Review
- Early construction of the thalamocortical axon pathway requires c-Jun N-terminal kinase signaling within the ventral forebrain.Developmental dynamics : an official publication of the American Association of Anatomists · 2022Article
- Review
- Epigenetic adaptations of the masticatory mucosa to periodontal inflammation.Clinical epigenetics · 2021Article
- Epithelial cell-turnover ensures robust coordination of tissue growth in Drosophila ribosomal protein mutants.PLoS genetics · 2021Article
- Kynurenine Metabolism in the Fat Body Non-autonomously Regulates Imaginal Disc Repair iniScience · 2020Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multicellular organisms repair injured epithelium by evolutionarily conserved biological processes including activation of c-Jun N-terminal kinase (JNK) signaling. Here, we show in Drosophila imaginal epithelium that physical injury leads to the emergence of dying cells, which are extruded from the wounded tissue by JNK-induced Slit-Roundabout2 (Robo2) repulsive signaling. Reducing Slit-Robo2 signaling in the wounded tissue suppresses extrusion of dying cells and generates aberrant cells with highly upregulated growth factors Wingless (Wg) and Decapentaplegic (Dpp). The inappropriately elevated Wg and Dpp impairs wound repair, as halving one of these growth factor genes cancelled wound healing defects caused by Slit-Robo2 downregulation. Our data suggest that JNK-mediated Slit-Robo2 signaling contributes to epithelial wound repair by promoting extrusion of dying cells from the wounded tissue, which facilitates transient and appropriate induction of growth factors for proper wound healing.
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