Journal
NATURE CELL BIOLOGY
Volume 19, Issue 3, Pages 155-163Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ncb3472
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Funding
- Marine Biological Laboratory (MBL, USA)
- National Institute of Arthritis and Musculoskeletal and Skin Disease (NIAMS), NIH [5R01AR063663-04, 1R01AR067755-01A1]
- Mallinckrodt Scholar Award
- James Hudson Brown-Alexander Brown Coxe Postdoctoral Fellowship
- CT Stem Cell Grant [14-SCA-YALE-05, 13-SCA-YALE-20]
- Yale Rheumatic Disease Research Core Center [P30 AR053495-08]
- NIH Predoctoral Program in Cellular and Molecular Biology [T32GM007223]
- National Institutes of Health [T32 GM007499]
- Canadian Institutes of Health Research Postdoctoral Fellowship
- CNRS
- INSERM
- Institut Curie
- ERC Advanced (TiMoprh) [340784]
- ARC [SL220130607097]
- ANR Labex DEEP [11-LBX-0044, ANR-10-IDEX-0001-02]
- PSL grants
- European Research Council (ERC) [340784] Funding Source: European Research Council (ERC)
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Tissue repair is fundamental to our survival as tissues are challenged by recurrent damage. During mammalian skin repair, cells respond by migrating and proliferating to close the wound. However, the coordination of cellular repair behaviours and their effects on homeostatic functions in a live mammal remains unclear. Here we capture the spatiotemporal dynamics of individual epithelial behaviours by imaging wound re-epithelialization in live mice. Differentiated cells migrate while the rate of differentiation changes depending on local rate of migration and tissue architecture. Cells depart from a highly proliferative zone by directionally dividing towards the wound while collectively migrating. This regional coexistence of proliferation and migration leads to local expansion and elongation of the repairing epithelium. Finally, proliferation functions to pattern and restrict the recruitment of undamaged cells. This study elucidates the interplay of cellular repair behaviours and consequent changes in homeostatic behaviours that support tissue-scale organization of wound re-epithelialization.
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