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Nat Cell Biol. 2017 Mar 1;19(2):155-163. doi: 10.1038/ncb3472. [Epub ahead of print]

Tissue-scale coordination of cellular behaviour promotes epidermal wound repair in live mice.

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Department of Genetics, Yale School of Medicine, New Haven, Connecticut 06510, USA.
Department of Laboratory Medicine, Department of Immunobiology, Yale School of Medicine, New Haven, Connecticut 06510, USA.
Polarity, Division and Morphogenesis Team, Genetics and Developmental Biology Unit (CNRS UMR3215/Inserm U934), Institut Curie, 75248 Paris Cedex 05, France.
Departments of Cell Biology and Dermatology, Yale Stem Cell Center, Yale Cancer Center, Yale School of Medicine, New Haven, Connecticut 06510, USA.


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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