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Title: JNK-mediated Slit-Robo signaling facilitates epithelial wound repair by extruding dying cells
Authors: Iida, Chiaki
Ohsawa, Shizue
Taniguchi, Kiichiro
Yamamoto, Masatoshi
Morata, Ginés
Igaki, Tatsushi  kyouindb  KAKEN_id
Author's alias: 飯田, 千晶
大澤, 志津江
谷口, 喜一郎
山本, 真寿
井垣, 達吏
Keywords: Extracellular signalling molecules
Stress signalling
Issue Date: 20-Dec-2019
Publisher: Springer Nature
Journal title: Scientific Reports
Volume: 9
Thesis number: 19549
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.
Rights: © The Author(s) 2019. This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
URI: http://hdl.handle.net/2433/246685
DOI(Published Version): 10.1038/s41598-019-56137-z
PubMed ID: 31863086
Appears in Collections:Journal Articles

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