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Loss of FMRP leads to fragile X syndrome (FXS), a common inherited form of intellectual disability and autism. While most research has been focusing on the neuronal contribution to FXS pathophysiology, the role of glia, particularly oligodendrocytes, is largely unknown. FXS individuals are characterized by white matter changes, which imply impairments in oligodendrocyte differentiation and myelination. We hypothesized that FMRP regulates oligodendrocyte maturation and myelination during postnatal development. Using a combination of human pluripotent stem cell\u2014derived oligodendrocytes and an\n                    <jats:italic>Fmr1<\/jats:italic>\n                    knockout rat model, we studied the role of FMRP on mammalian oligodendrocyte development. We found that the loss of FMRP leads to shared defects in oligodendrocyte morphology in both rat and human systems in\u00a0vitro, which persist in the presence of FMRP\u2010expressing axons in chimeric engraftment models. Our findings point to species\u2010conserved, cell\u2010autonomous defects during oligodendrocyte maturation in FXS.\n                  <\/jats:p>","DOI":"10.1002\/glia.24680","type":"journal-article","created":{"date-parts":[[2025,2,10]],"date-time":"2025-02-10T23:08:34Z","timestamp":1739228914000},"page":"1203-1220","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":7,"title":["The Fragile X Messenger Ribonucleoprotein 1 Regulates the Morphology and Maturation of Human and Rat Oligodendrocytes"],"prefix":"10.1002","volume":"73","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0375-7562","authenticated-orcid":false,"given":"Vidya","family":"Ramesh","sequence":"first","affiliation":[{"name":"Centre for Clinical Brain Sciences University of Edinburgh  Edinburgh UK"},{"name":"UK Dementia Research Institute University of Edinburgh  Edinburgh UK"},{"name":"Anne Rowling Regenerative Neurology Clinic (ARRNC) University of Edinburgh  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