Skin wound repair is essential to restore barrier function and prevent infection after tissue damage. Wound-edge epidermal cells migrate as a sheet to close the wound. However, it is still unclear how cell-cell junctions are regulated during wound closure (WC). To study this, we examined adherens junctions during WC in Drosophila larvae. β-catenin is reduced at the lateral cell-cell junctions of wound-edge epidermal cells in the early healing stages. Destruction complex components, including Ck1α, GSK3β and β-TrCP suppress β-catenin levels in the larval epidermis. Tissue-specific RNAi targeting these genes also caused severe WC defects. The Ck1αRNAi-induced WC defect is related to adherens junctions because loss of either β-catenin or E-cadherin significantly rescued this WC defect. In contrast, TCFRNAi does not rescue the Ck1αRNAi-induced WC defect, suggesting that Wnt signaling is not related to this defect. Direct overexpression of β-catenin recapitulates most of the features of Ck1α reduction during wounding. Finally, loss of Ck1α also blocked junctional E-cadherin reduction around the wound. Our results suggest that Ck1α and the destruction complex locally regulate cell adhesion to facilitate efficient wound repair.
Casein kinase 1α decreases β-catenin levels at adherens junctions to facilitate wound closure in Drosophila larvae
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Chang-Ru Tsai, Michael J. Galko; Casein kinase 1α decreases β-catenin levels at adherens junctions to facilitate wound closure in Drosophila larvae. Development 2019; dev.175133. doi: https://doi.org/10.1242/dev.175133
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