Polarized E-cadherin endocytosis directs actomyosin remodeling during embryonic wound repair.
Bottom Line: 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.Reducing E-cadherin levels in embryos in which endocytosis was blocked rescued actin localization to the wound margin.
Affiliation: Department of Cell and Systems Biology, University of Toronto, Toronto, Ontario M5S 3G5, Canada.Show MeSH
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Mentions: Our results showing that calcium is necessary for the polarization of the endocytic machinery to the wound margin predict that blocking calcium signaling should cause phenotypes similar to those resulting from blocking endocytosis. To investigate whether wound healing was delayed when we blocked calcium release, we measured the rate of wound closure in BAPTA-treated embryos (Fig. 6, A–D). Blocking calcium release led to wounds that closed at a rate of 11.9 ± 2.4 µm2/min, significantly slower than wounds in water-injected controls, which closed at a rate of 20.2 ± 3.4 µm2/min (P = 3.8 × 10−2; Fig. 6 D). We confirmed these results by treating embryos with 500 µM thapsigargin, a cell-permeable calcium chelator, which also delayed wound healing (Fig. S4, I and J). These data show that calcium release is necessary for rapid wound repair.
Affiliation: Department of Cell and Systems Biology, University of Toronto, Toronto, Ontario M5S 3G5, Canada.