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However, few well-defined stem cell markers have been identified for the analysis of FCSCs\u2019 cell fate and regulation mechanism. In this study, we first mapped the transcriptional landscape of the condylar cartilage and identified a Gli1+ subset. Label-retaining cells and our lineage-tracing study showed that Gli1 labeled a group of FCSCs. Conditional knockout \u03b2-catenin inhibited Gli1+ cells differentiating into hypertrophic chondrocytes. In discectomy-induced temporomandibular joint osteoarthritis (TMJOA), Gli1+ cells were further activated, and their differentiation into hypertrophic chondrocytes was accelerated, which induced stem cell pool depletion. The deletion of \u03b2-catenin in Gli1+ cells preserved the FCSC pool and alleviated TMJOA cartilage degeneration. Collectively, we uncovered that a Gli1+ FCSC subpopulation and Wnt\/\u03b2-catenin signaling orchestrate the Gli1+ cell fate in condyle postnatal development and TMJOA.<\/jats:p>","DOI":"10.1177\/00220345241274354","type":"journal-article","created":{"date-parts":[[2024,10,14]],"date-time":"2024-10-14T08:48:41Z","timestamp":1728895721000},"page":"1291-1301","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":22,"title":["\u03b2-catenin Orchestrates Gli1+ Cell Fate in Condylar Development and TMJOA"],"prefix":"10.1177","volume":"103","author":[{"ORCID":"https:\/\/orcid.org\/0009-0000-4988-5004","authenticated-orcid":false,"given":"J.","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Oral and Maxillofacial Surgery, Peking University School and Hospital of Stomatology & National Center for Stomatology & National Clinical Research Center for Oral Diseases & National Engineering Research Center of 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