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

Chang Ru Tsai, Michael J. Galko

Research output: Contribution to journalArticlepeer-review

5 Scopus citations

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 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.

Original languageEnglish (US)
Article numberdev175133
JournalDevelopment (Cambridge)
Volume146
Issue number20
DOIs
StatePublished - 2019

Keywords

  • Adherens junctions
  • Casein kinase 1α
  • Drosophila
  • Epithelium
  • Wound repair
  • β-Catenin

ASJC Scopus subject areas

  • Molecular Biology
  • Developmental Biology

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