Casein kinase 1α decreases β-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. 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 Ck1α^RNAi -induced WC defect is related to adherens junctions because loss of either β-catenin or E-cadherin significantly res

SUBMITTER: Tsai CR 

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

REPOSITORIES: biostudies-literature