ArticleMolecular autism2013
Common variation contributes to the genetic architecture of social communication traits.
Article in Molecular autism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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Who cites it
25 citing papers in PubMed, 46 citations in OpenAlex.
- Natural selection and language genes in humans.Scientific reports · 2026Article
- Disentangling multivariate relationships between cognition, language and social traits: structures of G, E, andbioRxiv : the preprint server for biology · 2025Article
- Translating Molecular Psychiatry: From Biomarkers to Personalized Therapies-A Narrative Review.International journal of molecular sciences · 2025Review
- Face perception and facial emotional expression recognition ability: Both unique predictors of the broader autism phenotype.Quarterly journal of experimental psychology (2006) · 2024Article
- Exome-wide analysis identify multiple variations in olfactory receptor genes (Frontiers in medicine · 2023Article
- A family-based study of genetic and epigenetic effects across multiple neurocognitive, motor, social-cognitive and social-behavioral functions.Behavioral and brain functions : BBF · 2022Article
- The DSM-5 introduction of the Social (Pragmatic) Communication Disorder as a new mental disorder: a philosophical review.History and philosophy of the life sciences · 2021Review
- MKRN3 regulates the epigenetic switch of mammalian puberty via ubiquitination of MBD3.National science review · 2020Article
- Rational use of mesenchymal stem cells in the treatment of autism spectrum disorders.World journal of stem cells · 2019Review
- Integrated genetic and methylomic analyses identify shared biology between autism and autistic traits.Molecular autism · 2019Article
- The other side of the coin: Hypersociability.Genes, brain, and behavior · 2019Review
- Quantitative trait locus mapping and analysis of heritable variation in affiliative social behavior and co-occurring traits.Genes, brain, and behavior · 2018Article
- Mendelian Randomization Analysis Identifies CpG Sites as Putative Mediators for Genetic Influences on Cardiovascular Disease Risk.American journal of human genetics · 2017Article
- Cellular and disease functions of the Prader-Willi Syndrome geneThe Biochemical journal · 2017Review
- A Comprehensive Guide to the MAGE Family of Ubiquitin Ligases.Journal of molecular biology · 2017Review
- A De Novo Nonsense Mutation in MAGEL2 in a Patient Initially Diagnosed as Opitz-C: Similarities Between Schaaf-Yang and Opitz-C Syndromes.Scientific reports · 2017Article
- Drosophila and genome-wide association studies: a review and resource for the functional dissection of human complex traits.Disease models & mechanisms · 2017Review
- VARPRISM: incorporating variant prioritization in tests of de novo mutation association.Genome medicine · 2016Article
- Article
- USP7 Acts as a Molecular Rheostat to Promote WASH-Dependent Endosomal Protein Recycling and Is Mutated in a Human Neurodevelopmental Disorder.Molecular cell · 2015Article
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 3 countries.
Funding
Abstract
backgroundSocial communication difficulties represent an autistic trait that is highly heritable and persistent during the course of development. However, little is known about the underlying genetic architecture of this phenotype.
methodsWe performed a genome-wide association study on parent-reported social communication problems using items of the children's communication checklist (age 10 to 11 years) studying single and/or joint marker effects. Analyses were conducted in a large UK population-based birth cohort (Avon Longitudinal Study of Parents and their Children, ALSPAC, N = 5,584) and followed-up within a sample of children with comparable measures from Western Australia (RAINE, N = 1364).
resultsTwo of our seven independent top signals (P-discovery <1.0E-05) were replicated (0.009 <P-replication ≤0.02) within RAINE and suggested evidence for association at 6p22.1 (rs9257616, meta-P = 2.5E-07) and 14q22.1 (rs2352908, meta-P = 1.1E-06). The signal at 6p22.1 was identified within the olfactory receptor gene cluster within the broader major histocompatibility complex (MHC) region. The strongest candidate locus within this genomic area was TRIM27. This gene encodes an ubiquitin E3 ligase, which is an interaction partner of methyl-CpG-binding domain (MBD) proteins, such as MBD3 and MBD4, and rare protein-coding mutations within MBD3 and MBD4 have been linked to autism. The signal at 14q22.1 was found within a gene-poor region.Single-variant findings were complemented by estimations of the narrow-sense heritability in ALSPAC suggesting that approximately a fifth of the phenotypic variance in social communication traits is accounted for by joint additive effects of genotyped single nucleotide polymorphisms throughout the genome (h2(SE) = 0.18(0.066), P = 0.0027).
conclusionOverall, our study provides both joint and single-SNP-based evidence for the contribution of common polymorphisms to variation in social communication phenotypes.
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.