ArticleCurrent biology : CB2011
A Gαq-Ca²⁺ signaling pathway promotes actin-mediated epidermal wound closure in C. elegans.
Article in Current biology : CB, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers.
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115 citing papers in PubMed.
- ATAD-3 couples plasma membrane injury to mitochondrial CaNature communications · 2026Article
- The basement membrane determines the choice of wound healing mechanism across wound scales in the basal eukaryoteMolecular biology of the cell · 2026Article
- Proton signaling links epithelial sensing to neural control of host defense in C. elegans.Nature communications · 2026Article
- Instant Membrane Stabilization by Damage-Triggered Actin Polymerization in Giant Unilamellar Vesicles.Chembiochem : a European journal of chemical biology · 2026Article
- Injury-induced electrochemical coupling triggers organ growth.Science advances · 2026Article
- Rules of life at the interface of calcium signaling and mechanobiology.APL bioengineering · 2025Review
- A steady-state pool of calcium-dependent actin is maintained by Homer and controls epithelial mechanosensation.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Cellular Adaptation to Mechanical Stress Emerges via Cell Shrinkage Triggered by Nonlinear Calcium Elevation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Actin mesh in Re-epithelialization during skin regeneration in adult newt (Regenerative therapy · 2025Article
- A knock-in translational reporter for NLP-29 reveals AMP secretion to the apical extracellular matrices following epidermal damage inmicroPublication biology · 2025Article
- Death-associated protein kinase 1: a double-edged sword in health and disease.Frontiers in immunology · 2025Review
- Calcium dynamics of skin-resident macrophages during homeostasis and tissue injury.Molecular biology of the cell · 2024Article
- Structural and physiological functions ofHeliyon · 2024Review
- Review
- Diverse calcium signaling profiles regulate migratory behavior in avascular wound healing and aberrant signal hierarchy occurs early in diabetes.American journal of physiology. Cell physiology · 2024Article
- Calcium dynamics of skin-resident macrophages during homeostasis and tissue injury.bioRxiv : the preprint server for biology · 2024Article
- The Caenorhabditis elegans cuticle and precuticle: a model for studying dynamic apical extracellular matrices in vivo.Genetics · 2024Review
- Cellular and molecular mechanisms of skin wound healing.Nature reviews. Molecular cell biology · 2024Review
- Time-course swRNA-seq uncovers a hierarchical gene regulatory network in controlling the response-repair-remodeling after wounding.Communications biology · 2024Article
- After wounding, a G-protein coupled receptor promotes the restoration of tension in epithelial cells.Molecular biology of the cell · 2024Article
55 more citing papers are in PubMed but not listed here.
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2 authors.
Funding
Abstract
backgroundRepair of skin wounds is essential for animals to survive in a harsh environment, yet the signaling pathways initiating wound repair in vivo remain little understood. In Caenorhabditis elegans, a p38 mitogen-activated protein kinase (MAPK) cascade promotes innate immune responses to wounding but is not required for other aspects of wound healing. We therefore set out to identify additional wound response pathways in C. elegans epidermis.
resultsWe show here that wounding the adult C. elegans skin triggers a rapid and sustained rise in epidermal Ca(2+) that is critical for survival after wounding. The wound-triggered rise in Ca(2+) requires the epidermal transient receptor potential channel, melastatin family (TRPM) channel GTL-2 and IP(3)R-stimulated release from internal stores. We identify an epidermal signal transduction pathway that includes the Gα(q) EGL-30 and its effector PLCβ EGL-8. Loss of function in this pathway impairs survival after wounding. The Gα(q)-Ca(2+) pathway is not required for known innate immune responses to wounding but instead promotes actin-dependent wound closure. Wound closure requires the Cdc42 small GTPase and Arp2/3-dependent actin polymerization and is negatively regulated by Rho and nonmuscle myosin. Finally, we show that the death-associated protein kinase DAPK-1 acts as a negative regulator of wound closure.
conclusionsSkin wounding in C. elegans triggers a Ca(2+)-dependent signaling cascade that promotes wound closure, in parallel to the innate immune response to damage. Wound closure requires actin polymerization and is negatively regulated by nonmuscle myosin.
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