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Hotspots of missense mutation identify neurodevelopmental disorder genes and functional domains
Journal article   Peer reviewed

Hotspots of missense mutation identify neurodevelopmental disorder genes and functional domains

Madeleine R Geisheker, Gabriel Heymann, Tianyun Wang, Bradley P Coe, Tychele N Turner, Holly A F Stessman, Kendra Hoekzema, Malin Kvarnung, Marie Shaw, Kathryn Friend, …
Nature neuroscience, Vol.20(8), pp.1043-1051
08/2017
DOI: 10.1038/nn.4589
PMCID: PMC5539915
PMID: 28628100
url
http://hdl.handle.net/1887/94670View
Open Access

Abstract

Although de novo missense mutations have been predicted to account for more cases of autism than gene-truncating mutations, most research has focused on the latter. We identified the properties of de novo missense mutations in patients with neurodevelopmental disorders (NDDs) and highlight 35 genes with excess missense mutations. Additionally, 40 amino acid sites were recurrently mutated in 36 genes, and targeted sequencing of 20 sites in 17,688 patients with NDD identified 21 new patients with identical missense mutations. One recurrent site substitution (p.A636T) occurs in a glutamate receptor subunit, GRIA1. This same amino acid substitution in the homologous but distinct mouse glutamate receptor subunit Grid2 is associated with Lurcher ataxia. Phenotypic follow-up in five individuals with GRIA1 mutations shows evidence of specific learning disabilities and autism. Overall, we find significant clustering of de novo mutations in 200 genes, highlighting specific functional domains and synaptic candidate genes important in NDD pathology.
Autistic Disorder - genetics Exome - genetics Genetic Predisposition to Disease Receptors, Glutamate - genetics Humans Female Male Amino Acid Sequence - genetics Receptors, AMPA - genetics Mutation, Missense - genetics

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