التفاصيل البيبلوغرافية
| العنوان: |
Polarized E-cadherin endocytosis directs actomyosin remodeling during embryonic wound repair. |
| المؤلفون: |
Hunter, Miranda V.1, Donghoon M. Lee1, Harris, Tony J. C.1, Fernandez-Gonzalez, Rodrigo1,2,3 rodrigo.fernandez.gonzalez@utoronto.ca |
| المصدر: |
Journal of Cell Biology. 8/31/2015, Vol. 210 Issue 5, p801-816. 16p. |
| مصطلحات موضوعية: |
*ENDOCYTOSIS, *CLATHRIN, *DYNAMIN (Genetics), *ADP-ribosylation factors, *DROSOPHILA melanogaster, *CELLULAR signal transduction, *ACTOMYOSIN, *CADHERINS, *INSECTS |
| مستخلص: |
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 . [ABSTRACT FROM AUTHOR] |
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