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The relationship between reduced or dysfunctional SMARCB1 protein products and severe functional brain changes associated with Coffin-Siris syndrome, including intellectual disability and severely delayed language and motor development, remains largely unknown. We performed cellular, molecular, and behavioural analyses of a Coffin-Siris syndrome mouse model with a heterozygous nervous system-specific\n                    <jats:italic>Smarcb1<\/jats:italic>\n                    mutation. In addition, we evaluated general cognitive abilities, as well as cognitive and behavioural functioning, in individuals with\n                    <jats:italic>SMARCB1<\/jats:italic>\n                    -related Coffin-Siris syndrome.\n                    <jats:italic>Smarcb1<\/jats:italic>\n                    mutant mice exhibited deficits in fine motor coordination and balance, as well as impaired spatial learning and memory. Furthermore, these mice showed anxiety-like behaviours and agitation when exposed to novel environments. The detected behavioural abnormalities could indicate impaired decision-making, which results in impaired risk assessment. Comparable cognitive and behavioural deviations were identified in individuals with Coffin-Siris syndrome and\n                    <jats:italic>SMARCB1<\/jats:italic>\n                    pathogenic variants. Histological analyses revealed structural alterations in the brain of the\n                    <jats:italic>Smarcb1<\/jats:italic>\n                    mouse model, including decreased dendritic length and complexity of dendritic trees. These alterations may explain the observed functional impairments. Notably, our finding of reduced\n                    <jats:italic>Wasl<\/jats:italic>\n                    transcripts in mutant Purkinje cell nuclei suggests that dysregulation of actin polymerization may be involved in the discovered dendritic defects. Taken together, we demonstrate a link between the chromatin remodelling complex component SMARCB1, complex brain functions, neuronal structure, and a key regulator of actin branching.\n                  <\/jats:p>","DOI":"10.1186\/s40478-026-02258-2","type":"journal-article","created":{"date-parts":[[2026,2,19]],"date-time":"2026-02-19T13:36:59Z","timestamp":1771508219000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Chromatin remodelling subunit SMARCB1 is implicated in dendrite development and complex brain functions"],"prefix":"10.1186","volume":"14","author":[{"given":"Kristina I.","family":"Lemke","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alina","family":"Filatova","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joanna","family":"Chiang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hannah","family":"North","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Myrthe R. 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