Polarized E-cadherin endocytosis directs actomyosin remodeling during embryonic wound repair

Miranda V. Hunter, Donghoon M. Lee, Tony J.C. Harris, Rodrigo Fernandez-Gonzalez

Research output: Contribution to journalArticlepeer-review

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.

Original languageEnglish (US)
Pages (from-to)801-816
Number of pages16
JournalJournal of Cell Biology
Volume210
Issue number5
DOIs
StatePublished - Aug 31 2015
Externally publishedYes

ASJC Scopus subject areas

  • Cell Biology

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