TY - JOUR
T1 - Polarized E-cadherin endocytosis directs actomyosin remodeling during embryonic wound repair
AU - Hunter, Miranda V.
AU - Lee, Donghoon M.
AU - Harris, Tony J.C.
AU - Fernandez-Gonzalez, Rodrigo
N1 - Funding Information:
This work was supported by a Connaught Fund New Investigator Award to R. Fernandez-Gonzalez and grants from the University of Toronto Faculty of Medicine Dean's New Staff Fund, the Canada Foundation for Innovation (#30279), and the Natural Sciences and Engineering Research Council of Canada Discovery Grant program (#418438-13) to R. Fernandez-Gonzalez.
Publisher Copyright:
© 2015 Hunter et al.
PY - 2015/8/31
Y1 - 2015/8/31
N2 - 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.
AB - 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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U2 - 10.1083/jcb.201501076
DO - 10.1083/jcb.201501076
M3 - Article
C2 - 26304727
AN - SCOPUS:84962168158
SN - 0021-9525
VL - 210
SP - 801
EP - 816
JO - Journal of Cell Biology
JF - Journal of Cell Biology
IS - 5
ER -