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In mice, the development of uterine gland known as adenogenesis occurs after birth, whereas the adenogenesis in humans initiates from fetal life and completed at puberty. Uterine adenogenesis involves dynamic epithelial cell proliferation, differentiation, and apoptosis. However, it is largely unexplored about the mechanisms governing adenogenesis. CK1\u03b1 plays important roles in regulating cell division, differentiation, and death, but it is unknown whether CK1\u03b1 affects adenogenesis. In the current study, uterus-specific CK1\u03b1 knockout female mice (Csnk1a1d\/d) were infertile resulted from lack of uterine glands. Subsequent analysis revealed that CK1\u03b1 deletion induced massive apoptosis in uterine epithelium by activating GSK3\u03b2, which was confirmed by injections of GSK3\u03b2 inhibitor SB216763 to Csnk1a1d\/d females, and the co-treatment of SB216763 and CK1 inhibitor d4476 on cultured epithelial cells. Another important finding was that our results revealed CK1\u03b1 deficiency activated p53, which then blocked the expression of Foxa2, an important factor for glandular epithelium development and function. This was confirmed by that Foxa2 expression level was elevated in p53 inhibitor pifithrin-\u03b1 injected Csnk1a1d\/d mouse uterus and in vitro dual-luciferase reporter assay between p53 and Foxa2. Collectively, these studies reveal that CK1\u03b1 is a novel factor regulating uterine adenogenesis by inhibiting epithelial cell apoptosis through GSK3\u03b2 pathway and regulating Foxa2 expression through p53 pathway. Uncovering the mechanisms of uterine adenogenesis is expected to improve pregnancy success in humans and other mammals.<\/jats:p>","DOI":"10.1093\/biolre\/ioad144","type":"journal-article","created":{"date-parts":[[2023,11,9]],"date-time":"2023-11-09T20:58:43Z","timestamp":1699563523000},"page":"246-260","source":"Crossref","is-referenced-by-count":3,"title":["CK1\u03b1 deficiency impairs mouse uterine adenogenesis by inducing epithelial cell apoptosis through GSK3\u03b2 pathway and inhibiting Foxa2 expression through p53 pathway"],"prefix":"10.1093","volume":"110","author":[{"given":"Di","family":"Zhang","sequence":"first","affiliation":[{"name":"College of Veterinary Medicine, Yangzhou University , Yangzhou, Jiangsu , People\u2019s Republic of China"},{"name":"Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou University , Yangzhou , People\u2019s Republic of China"},{"name":"Institute of Reproduction and Metabolism, 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