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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. \u03b2-catenin is reduced at the lateral cell-cell junctions of wound-edge epidermal cells in the early healing stages. Destruction complex components, including Ck1\u03b1, GSK3\u03b2 and \u03b2-TrCP suppress \u03b2-catenin levels in the larval epidermis. Tissue-specific RNAi targeting these genes also caused severe WC defects. The Ck1\u03b1RNAi-induced WC defect is related to adherens junctions because loss of either \u03b2-catenin or E-cadherin significantly rescued this WC defect. In contrast, TCFRNAi does not rescue the Ck1\u03b1RNAi-induced WC defect, suggesting that Wnt signaling is not related to this defect. Direct overexpression of \u03b2-catenin recapitulates most of the features of Ck1\u03b1 reduction during wounding. Finally, loss of Ck1\u03b1 also blocked junctional E-cadherin reduction around the wound. Our results suggest that Ck1\u03b1 and the destruction complex locally regulate cell adhesion to facilitate efficient wound repair.<\/jats:p>","DOI":"10.1242\/dev.175133","type":"journal-article","created":{"date-parts":[[2019,9,11]],"date-time":"2019-09-11T14:55:16Z","timestamp":1568213716000},"source":"Crossref","is-referenced-by-count":5,"title":["Casein kinase 1\u03b1 decreases \u03b2-catenin levels at adherens junctions to facilitate wound closure in<i>Drosophila<\/i>larvae"],"prefix":"10.1242","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5672-1235","authenticated-orcid":false,"given":"Chang-Ru","family":"Tsai","sequence":"first","affiliation":[{"name":"Program in Developmental Biology, Baylor College of Medicine, Houston, Texas, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3759-2017","authenticated-orcid":false,"given":"Michael J.","family":"Galko","sequence":"additional","affiliation":[{"name":"Program in Developmental Biology, Baylor College of Medicine, Houston, Texas, USA"},{"name":"Department of Genetics, University of Texas MD Anderson Cancer Center, Houston, Texas, USA"},{"name":"Genetics & Epigenetics Graduate Program, University of Texas MD Anderson Cancer Center, Houston, Texas, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"237","published-online":{"date-parts":[[2019,1,1]]},"reference":[{"key":"2021042623490412300_DEV175133C1","doi-asserted-by":"publisher","first-page":"3797","DOI":"10.1093\/emboj\/16.13.3797","article-title":"beta-catenin is a target for the ubiquitin-proteasome pathway","volume":"16","author":"Aberle","year":"1997","journal-title":"EMBO J."},{"key":"2021042623490412300_DEV175133C2","doi-asserted-by":"publisher","first-page":"5984","DOI":"10.1242\/jcs.109066","article-title":"Drosophila embryos close epithelial wounds using a combination of cellular protrusions and an actomyosin purse string","volume":"125","author":"Abreu-Blanco","year":"2013","journal-title":"J. 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