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KIF2A, encoding a kinesin-13 microtubule-depolymerase, is associated with a rare autosomal dominant cortical dysplasia syndrome (CDCBM3). A single unrelated 8-year-old boy presented with posterior dominant agyria/pachygyria and motor dysfunction and harbored a de novo heterozygous NM_001098511.2:c.1298C>A (p.Ser433Tyr) variant, located distal to the nucleotide-binding domain in line with CDCBM3 mutation spectrum (PMID:33506645). No additional familial segregation has been reported.
Multiple functional studies reinforce a dominant-negative mechanism: de novo motor domain substitutions c.950G>A (p.Ser317Asn) and c.962A>C (p.His321Pro) disrupt ATP hydrolysis and microtubule depolymerization, causing lissencephaly and microcephaly (PMID:27747449). Cell models show impaired progenitor proliferation, neuron migration, and ciliogenesis–cell cycle coupling (PMID:29077851). Conditional KIF2A p.His321Asp knock-in mice recapitulate microcephaly, cortical malformation, increased apoptosis, and neuronal differentiation defects (PMID:31919497). Although clinical data are limited to one proband, the concordant functional evidence supports pathogenicity. Key take-home: consider KIF2A testing in patients with agyria/pachygyria and motor deficits.
Gene–Disease AssociationLimitedSingle unrelated proband with de novo heterozygous variant and no segregation evidence Genetic EvidenceLimitedOne proband with de novo c.1298C>A (p.Ser433Tyr) variant in KIF2A with no additional familial segregation ([PMID:33506645]) Functional EvidenceModerateMultiple functional studies, including patient-derived cell assays and knock-in mouse models, demonstrate KIF2A variant-induced microtubule depolymerization defects and cortical malformations ([PMID:27747449], [PMID:29077851], [PMID:31919497]) |