Polarized E-cadherin endocytosis directs actomyosin remodeling during embryonic wound repair.
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| Abstract |
Embryonic epithelia have a remarkable ability to rapidly repair wounds. A supracellular actomyosin cable around the wound coordinates cellular movements and promotes wound closure. Actomyosin cable formation is accompanied by junctional rearrangements at the wound margin. We used in vivo time-lapse quantitative microscopy to show that clathrin, dynamin, and the ADP-ribosylation factor 6, three components of the endocytic machinery, accumulate around wounds in Drosophila melanogaster embryos in a process that requires calcium signaling and actomyosin contractility. Blocking endocytosis with pharmacological or genetic approaches disrupted wound repair. The defect in wound closure was accompanied by impaired removal of E-cadherin from the wound edge and defective actomyosin cable assembly. E-cadherin overexpression also resulted in reduced actin accumulation around wounds and slower wound closure. Reducing E-cadherin levels in embryos in which endocytosis was blocked rescued actin localization to the wound margin. Our results demonstrate a central role for endocytosis in wound healing and indicate that polarized E-cadherin endocytosis is necessary for actomyosin remodeling during embryonic wound repair.
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| Authors | Miranda V Hunter, Donghoon M Lee, Tony J C Harris, Rodrigo Fernandez-Gonzalez |
| Journal | The Journal of cell biology (J Cell Biol) Vol. 210 Issue 5 Pg. 801-16 (Aug 31 2015) ISSN: 1540-8140 [Electronic] United States |
| PMID | 26304727 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't) |
| Copyright | © 2015 Hunter et al. |
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