RRC ID 58240
Author Iida C, Ohsawa S, Taniguchi K, Yamamoto M, Morata G, Igaki T.
Title JNK-mediated Slit-Robo signaling facilitates epithelial wound repair by extruding dying cells.
Journal Sci Rep
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.
Volume 9(1)
Pages 19549
Published 2019-12-20
DOI 10.1038/s41598-019-56137-z
PII 10.1038/s41598-019-56137-z
PMID 31863086
PMC PMC6925126
MeSH Animals Drosophila / genetics Drosophila / metabolism* Drosophila Proteins / genetics Drosophila Proteins / metabolism* JNK Mitogen-Activated Protein Kinases / genetics JNK Mitogen-Activated Protein Kinases / metabolism* Receptors, Immunologic / genetics Receptors, Immunologic / metabolism Signal Transduction / physiology* Wnt1 Protein / genetics Wnt1 Protein / metabolism Wound Healing / genetics Wound Healing / physiology
IF 3.998
Times Cited 0
Drosophila 5680R-2 DGRC#106948 DGRC#106843 DGRC#106646 DGRC#106649