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However, the mechanisms by which\n                    <jats:italic>WNT16<\/jats:italic>\n                    promotes bone health and repair are not fully understood. In this study, CRISPR\u2010Cas9 was used to generate mutant zebrafish lacking Wnt16 (\n                    <jats:italic>wnt16<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>\u2212\/\u2212<\/jats:italic>\n                    <\/jats:sup>\n                    ) to study its effect on bone dynamically. The\n                    <jats:italic>wnt16<\/jats:italic>\n                    mutants displayed variable tissue mineral density (TMD) and were susceptible to spontaneous fractures and the accumulation of bone calluses at an early age. Fractures were induced in the lepidotrichia of the caudal fins of\n                    <jats:italic>wnt16<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>\u2212\/\u2212<\/jats:italic>\n                    <\/jats:sup>\n                    and WT zebrafish; this model was used to probe the mechanisms by which Wnt16 regulates skeletal and immune cell dynamics\n                    <jats:italic>in vivo<\/jats:italic>\n                    . In WT fins,\n                    <jats:italic>wnt16<\/jats:italic>\n                    expression increased significantly during the early stages for bone repair. Mineralization of bone during fracture repair was significantly delayed in\n                    <jats:italic>wnt16<\/jats:italic>\n                    mutants compared with WT zebrafish. Surprisingly, there was no evidence that the recruitment of innate immune cells to fractures or soft callus formation was altered in\n                    <jats:italic>wnt16<\/jats:italic>\n                    mutants. However, osteoblast recruitment was significantly delayed in\n                    <jats:italic>wnt16<\/jats:italic>\n                    mutants postfracture, coinciding with precocious activation of the canonical Wnt signaling pathway.\n                    <jats:italic>In situ<\/jats:italic>\n                    hybridization suggests that canonical Wnt\u2010responsive cells within fractures are osteoblast progenitors, and that osteoblast differentiation during bone repair is coordinated by the dynamic expression of\n                    <jats:italic>runx2a<\/jats:italic>\n                    and\n                    <jats:italic>wnt16<\/jats:italic>\n                    . This study highlights zebrafish as an emerging model for functionally validating osteoporosis\u2013associated genes and investigating fracture repair dynamically\n                    <jats:italic>in vivo<\/jats:italic>\n                    . Using this model, it was found that Wnt16 protects against fracture and supports bone repair, likely by modulating canonical Wnt activity via\n                    <jats:italic>runx2a<\/jats:italic>\n                    to facilitate osteoblast differentiation and bone matrix deposition. \u00a9 2021 The Authors.\n                    <jats:italic>JBMR Plus<\/jats:italic>\n                    published by Wiley Periodicals LLC. on behalf of American Society for Bone and Mineral Research.\n                  <\/jats:p>","DOI":"10.1002\/jbm4.10461","type":"journal-article","created":{"date-parts":[[2021,1,15]],"date-time":"2021-01-15T05:00:53Z","timestamp":1610686853000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":33,"title":["Wnt16 Elicits a Protective Effect Against Fractures and Supports Bone Repair in Zebrafish"],"prefix":"10.1093","volume":"5","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5576-605X","authenticated-orcid":false,"given":"Lucy M","family":"McGowan","sequence":"first","affiliation":[{"name":"School of Physiology, Pharmacology and Neuroscience University of Bristol  Bristol UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0266-9424","authenticated-orcid":false,"given":"Erika","family":"Kague","sequence":"additional","affiliation":[{"name":"School of Physiology, Pharmacology and Neuroscience University of Bristol  Bristol UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alistair","family":"Vorster","sequence":"additional","affiliation":[{"name":"School of Physiology, Pharmacology and Neuroscience University of Bristol  Bristol UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elis","family":"Newham","sequence":"additional","affiliation":[{"name":"School of Physiology, Pharmacology and Neuroscience University of Bristol  Bristol UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3565-0479","authenticated-orcid":false,"given":"Stephen","family":"Cross","sequence":"additional","affiliation":[{"name":"Wolfson Bioimaging Facility University of Bristol  Bristol UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4935-6724","authenticated-orcid":false,"given":"Chrissy L","family":"Hammond","sequence":"additional","affiliation":[{"name":"School of Physiology, Pharmacology and Neuroscience University of Bristol  Bristol UK"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2021,2,2]]},"reference":[{"key":"e_1_2_9_2_1","doi-asserted-by":"publisher","DOI":"10.7150\/ijbs.27063"},{"key":"e_1_2_9_3_1","doi-asserted-by":"publisher","DOI":"10.1002\/jbmr.2735"},{"key":"e_1_2_9_4_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.clinthera.2015.06.006"},{"key":"e_1_2_9_5_1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.R109.041087"},{"key":"e_1_2_9_6_1","doi-asserted-by":"publisher","DOI":"10.1359\/JBMR.050304"},{"key":"e_1_2_9_7_1","unstructured":"National Osteoporosis Society.NHS right care scenario: the variation between sub\u2010optimal and optimal pathways. 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