Casein kinase 1? decreases ?-catenin levels at adherens junctions to facilitate wound closure in Drosophila larvae.

ABSTRACT: 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. ?-Catenin is reduced at the lateral cell-cell junctions of wound-edge epidermal cells in the early healing stages. Destruction complex components, including Ck1?, GSK3? and ?-TrCP, suppress ?-catenin levels in the larval epidermis. Tissue-specific RNAi targeting these genes also caused severe WC defects. The Ck1?^RNAi -induced WC defect is related to adherens junctions because loss of either ?-catenin or E-cadherin significantly rescued this WC defect. In contrast, TCF^RNAi does not rescue the Ck1?^RNAi -induced WC defect, suggesting that Wnt signaling is not related to this defect. Direct overexpression of ?-catenin recapitulates most of the features of Ck1? reduction during wounding. Finally, loss of Ck1? also blocked junctional E-cadherin reduction around the wound. Our results suggest that Ck1? and the destruction complex locally regulate cell adhesion to facilitate efficient wound repair.

SUBMITTER: Tsai CR 

PROVIDER: S-EPMC6826034 | biostudies-literature | 2019 Oct

REPOSITORIES: biostudies-literature