p38-mediated cell growth and survival drive rapid embryonic wound repair

• DOI: 10.1016/j.celrep.2021.109874
• Publication Date: 2021-10-22T06:57:29Z
• Authors: Gordana Scepanovic; Miranda Victoria ...; Ran Kafri; Rodrigo Fernandez...
• Keywords: 0301 basic medicine; Time Factors; quantitative image analysis; QH301-705.5; wound healing; p38 Mitogen-Activated Protein Kinases; Animals, Genetically Modified; 03 medical and health sciences; Animals; Drosophila Proteins; Solute Carrier Family 12, Member 2; Biology (General); cell volume; Cell Proliferation; Cell Size; reactive oxygen species; Myosin Type II; Wound Healing; collective cell migration; epithelial morphogenesis; Gene Expression Regulation, Developmental; Enzyme Activation; Oxidative Stress; Drosophila melanogaster; Wounds and Injuries; Reactive Oxygen Species; Signal Transduction

Embryos repair wounds rapidly, with no inflammation or scarring, in a process that involves polarization of the actomyosin cytoskeleton. Actomyosin polarization results in the assembly of a contractile cable around the wound that drives wound closure. Here, we demonstrate that a contractile actomyosin cable is not sufficient for rapid wound repair in Drosophila embryos. We show that wounding causes activation of the serine/threonine kinase p38 mitogen-activated protein kinase (MAPK) in the cells adjacent to the wound. p38 activation reduces the levels of wound-induced reactive oxygen species in the cells around the wound, limiting wound size. In addition, p38 promotes an increase in volume in the cells around the wound, thus facilitating the collective cell movements that drive rapid wound healing. Our data indicate that p38 regulates cell volumes through the sodium-potassium-chloride cotransporter NKCC1. Our work reveals cell growth and cell survival as cell behaviors critical for embryonic wound repair.