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Distinct sub-clusters of developmental disorder-associated variants in the switch II region of RAC1
Journal article   Open access   Peer reviewed

Distinct sub-clusters of developmental disorder-associated variants in the switch II region of RAC1

Hebah O Althebaiti, James Cooksedge, Martin J Baker, Madeleine Smith, Verity Edwards-Scott, André Luiz Santos Pessoa, Henri Margot, Kay A Metcalfe, Mélanie Fradin, Hailey Mostow, …
European journal of human genetics : EJHG
12 May 2026
PMID: 42120539
url
https://doi.org/10.1038/s41431-026-02105-xView
Published, Version of Record (VoR) Open

Abstract

RAC1 is a signal transducer essential for neurodevelopment. Missense variants in RAC1 cause heterogeneous neurodevelopmental disorders whose features include intellectual disability and developmental delay. Individuals with RAC1 variants are categorized by head circumference into microcephalic, normocephalic and macrocephalic groups. We previously described a cohort of individuals with variants affecting the N-terminal part (Q61-R68) of switch II, a functional domain of RAC1. This cohort was normocephalic and their variants increased RAC1 signalling activity. Here, we report 15 new individuals with variants in switch II of RAC1. We describe clinical features for two individuals with variants affecting the N-terminal part of switch II (Q61-R68) and four individuals with variants in its C-terminal part (P69-Q74). All individuals exhibit intellectual disabilities and neuroradiological anomalies. Consistent with our previous study, individuals with variants in the N-terminal part of switch II were normocephalic. By contrast, individuals with variants in the C-terminal part of switch II exhibited microcephaly. Cell-based assays revealed that N- and C-terminal variants affect RAC1 function differently: N-terminal variants are activating, while C-terminal variants are dominant-negative. In a Drosophila model, we observe divergent effects on neuronal morphology, with switch II N-terminal variants increasing the complexity of dendritic arbors, while switch II C-terminal variants reduce dendritic complexity. Switch II N-terminal variants increase locomotor activity of adult Drosophila, while C-terminal variants had minimal effect, suggesting diverging effects on neuronal function and behaviour. We conclude that variants affecting N- and C-terminal parts of RAC1 switch II cause phenotypically and mechanistically distinct disorders.

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Collaboration types
Domestic collaboration
International collaboration
Web of Science research areas
Biochemistry & Molecular Biology
Genetics & Heredity
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