Variant Synonymizer: Platform to identify mutations defined in different ways is available now!
Over 2,000 gene–disease validation summaries are now available—no login required!
Rare copy-number variants disrupting CNTN4 have been reported in individuals with autism spectrum disorder. Array-based CGH identified a paternally inherited deletion in two siblings and a duplication in a third unrelated case, with Alu Y–mediated breakpoints interrupting CNTN4 (PMID:18349135). Subsequent screening of three unrelated families revealed one additional deletion and two duplications within CNTN4, all paternally derived and associated with ASD, cognitive delay, motor delay (HP:0001270), and speech impairment, demonstrating variable expressivity and incomplete penetrance (PMID:31422286). No recurrent coding variants have been described.
Genome-wide studies in East Asian and European cohorts provided nominal association signals for CNTN4 in case-control and family-based analyses, but these did not reach genome-wide significance and lacked replication across populations (PMID:26314684; PMID:19404257). Segregation is limited to two affected siblings in one family, and other familial CNVs do not co-segregate consistently. Contactin 4 is a neuronal cell-adhesion molecule critical for synaptic network formation and plasticity, offering biological plausibility for ASD when disrupted, yet direct functional assays of CNTN4 variants in ASD models are lacking (PMID:18349135).
Key Take-home: Rare CNTN4 CNVs and nominal association signals support a limited role for CNTN4 in ASD risk, warranting further genetic and functional investigation.
Gene–Disease AssociationLimitedCNVs in 6 probands across two case series (PMID:18349135; PMID:31422286) and nominal association in GWAS (PMID:26314684; PMID:19404257) but lacking consistent segregation and replication Genetic EvidenceLimitedMultiple rare CNTN4 CNVs in unrelated ASD cases (total n=6) and nominal association signals in population studies Functional EvidenceLimitedCNTN4’s role in neuronal network formation is biologically plausible for ASD but direct functional assays of ASD-associated variants are lacking |