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The development and maturation of the enthesis involve cellular processes likened to an arrested growth plate. In this study, we explored the role of fibroblast growth factor 9 (\n                    <jats:italic>Fgf9<\/jats:italic>\n                    ), a known regulator of chondrogenesis and vascularization during bone development, on the structure and function of the postnatal enthesis. First, we confirmed spatial expression of\n                    <jats:italic>Fgf9<\/jats:italic>\n                    in the tendon and enthesis using in situ hybridization. We then used Cre\u2010lox recombinase to conditionally knockout\n                    <jats:italic>Fgf9<\/jats:italic>\n                    in mouse tendon and enthesis (\n                    <jats:italic>Scx\u2010Cre<\/jats:italic>\n                    ) and characterized enthesis morphology as well as mechanical properties in\n                    <jats:italic>Fgf9<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>ScxCre<\/jats:italic>\n                    <\/jats:sup>\n                    and wild\u2010type (WT) entheses.\n                    <jats:italic>Fgf9<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>ScxCre<\/jats:italic>\n                    <\/jats:sup>\n                    mice had smaller calcaneal and humeral apophyses, thinner cortical bone at the attachment, increased cellularity, and reduced failure load in mature entheses compared to WT littermates. During postnatal development, we found reduced chondrocyte hypertrophy and disrupted type X collagen (Col X) in\n                    <jats:italic>Fgf9<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>ScxCre<\/jats:italic>\n                    <\/jats:sup>\n                    entheses. These findings support that tendon\u2010derived\n                    <jats:italic>Fgf9<\/jats:italic>\n                    is important for functional development of the enthesis, including its postnatal mineralization. Our findings suggest the potential role of FGF signaling during enthesis development.\n                  <\/jats:p>","DOI":"10.1096\/fj.202201614r","type":"journal-article","created":{"date-parts":[[2023,2,3]],"date-time":"2023-02-03T10:09:22Z","timestamp":1675418962000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["Targeted deletion of\n                    <i>Fgf9<\/i>\n                    in tendon disrupts mineralization of the developing enthesis"],"prefix":"10.1096","volume":"37","author":[{"given":"Elahe","family":"Ganji","sequence":"first","affiliation":[{"name":"Department of Orthopaedic Surgery Michigan Medicine  Michigan Ann Arbor USA"},{"name":"Department of Mechanical Engineering University of Delaware  Delaware Newark USA"},{"name":"Beckman Institute for Advanced Science and Technology University of Illinois at Urbana\u2010Champaign  61801 IL Urbana United\u00a0States"},{"name":"Department of Biomedical Engineering University of Delaware  Delaware Newark USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Connor","family":"Leek","sequence":"additional","affiliation":[{"name":"Department of Orthopaedic Surgery Michigan Medicine  Michigan Ann Arbor USA"},{"name":"Department of Biomedical Engineering University of Delaware  Delaware Newark USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"William","family":"Duncan","sequence":"additional","affiliation":[{"name":"Department of Biomedical Engineering University of Delaware  Delaware Newark USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Debabrata","family":"Patra","sequence":"additional","affiliation":[{"name":"Department of Developmental Biology Washington University School of Medicine  Missouri St Louis USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1592-7629","authenticated-orcid":false,"given":"David 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