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Their activities are downregulated by GTPase\u2010activating proteins (GAPs). Although RhoGTPases are implicated in bone remodeling and osteoclast and osteoblast function, their significance in human bone health and disease remains elusive. Here, we report defective RhoGTPase regulation as a cause of severe, early\u2010onset, autosomal\u2010dominant skeletal fragility in a three\u2010generation Finnish family. Affected individuals (\n                    <jats:italic>n<\/jats:italic>\n                    \u00a0=\u00a013) presented with multiple low\u2010energy peripheral and vertebral fractures despite normal bone mineral density (BMD). Bone histomorphometry suggested reduced bone volume, low surface area covered by osteoblasts and osteoclasts, and low bone turnover. Exome sequencing identified a novel heterozygous missense variant c.652G&gt;A (p.G218R) in\n                    <jats:italic>ARHGAP25<\/jats:italic>\n                    , encoding a GAP for Rho\u2010family GTPase Rac1. Variants in the\n                    <jats:italic>ARHGAP25<\/jats:italic>\n                    5\u2032 untranslated region (UTR) also associated with BMD and fracture risk in the general population, across multiple genomewide association study (GWAS) meta\u2010analyses (lead variant rs10048745).\n                    <jats:italic>ARHGAP25<\/jats:italic>\n                    messenger RNA (mRNA) was expressed in macrophage colony\u2010stimulating factor (M\u2010CSF)\u2013stimulated human monocytes and mouse osteoblasts, indicating a possible role for ARHGAP25 in osteoclast and osteoblast differentiation and activity. Studies on subject\u2010derived osteoclasts from peripheral blood mononuclear cells did not reveal robust defects in mature osteoclast formation or resorptive activity. However, analysis of osteosarcoma cells overexpressing the ARHGAP25 G218R\u2010mutant, combined with structural modeling, confirmed that the mutant protein had decreased GAP\u2010activity against Rac1, resulting in elevated Rac1 activity, increased cell spreading, and membrane ruffling. Our findings indicate that mutated ARHGAP25 causes aberrant Rac1 function and consequently abnormal bone metabolism, highlighting the importance of RhoGAP signaling in bone metabolism in familial forms of skeletal fragility and in the general population, and expanding our understanding of the molecular pathways underlying skeletal fragility. \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\/jbm4.10509","type":"journal-article","created":{"date-parts":[[2021,5,6]],"date-time":"2021-05-06T18:28:06Z","timestamp":1620325686000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":15,"title":["An\n                    <scp>\n                      <i>ARHGAP25<\/i>\n                    <\/scp>\n                    variant links aberrant\n                    <scp>Rac1<\/scp>\n                    function to early\u2010onset skeletal fragility"],"prefix":"10.1093","volume":"5","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2907-3348","authenticated-orcid":false,"given":"Riikka E.","family":"M\u00e4kitie","sequence":"first","affiliation":[{"name":"Folkh\u00e4lsan Institute of Genetics Helsinki Finland"},{"name":"Research Program for Clinical and Molecular Metabolism, Faculty of Medicine University of Helsinki Helsinki Finland"},{"name":"Molecular Endocrinology Laboratory, Department of Metabolism, Digestion and Reproduction Imperial College London London UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Petra","family":"Henning","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine and Clinical Nutrition Centre for Bone and Arthritis Research, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg Gothenburg Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yaming","family":"Jiu","sequence":"additional","affiliation":[{"name":"HiLIFE Institute of Biotechnology University of Helsinki Helsinki Finland"},{"name":"The Center for Microbes, Development and Health, Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai Chinese Academy of Sciences Shanghai China"},{"name":"University of Chinese Academy of Sciences Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1829-3855","authenticated-orcid":false,"given":"Anders","family":"K\u00e4mpe","sequence":"additional","affiliation":[{"name":"Department of Molecular Medicine and Surgery and Center for Molecular Medicine Karolinska Institutet Stockholm Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Konstantin","family":"Kogan","sequence":"additional","affiliation":[{"name":"HiLIFE Institute of Biotechnology University of 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