ArticleScience China. Life sciences2024
Whole-genome sequencing identifies novel genes for autism in Chinese trios.
Article in Science China. Life sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed.
- Heterozygous Variants in LRP1 Cause a Neurodevelopmental Disorder With Congenital Heart Defects.American journal of medical genetics. Part A · 2026Article
- Characterization of rare genomic structural variants across 2,981 genomes reveals significant involvements in recessive conditions.Science China. Life sciences · 2026Article
- Decomposing the genetic risk of autism spectrum disorder into discrete molecular subtypes underlie clinical heterogeneity based on transcriptome profile.Journal of translational medicine · 2026Article
- Deficiency of primate-specific TFDP3 causes male infertility with oligoasthenoteratozoospermia in humans and cynomolgus monkeys.Science China. Life sciences · 2026Article
- Transcriptomic analysis in autism spectrum disorder suggests three molecular subtypes with distinct phenotypic profiles and functional pathways.Communications biology · 2026Article
- Sh3rf3 Deficiency drives autism-like behaviors via presynaptic dysfunction in mice.Molecular psychiatry · 2026Article
- ZNRF3 in neurodevelopmental disorders: insights into Wnt signaling and therapeutic potential.Neurogenetics · 2025Review
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13 authors.
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Abstract
Autism spectrum disorder (ASD) is a neurodevelopmental disorder with high genetic heritability but heterogeneity. Fully understanding its genetics requires whole-genome sequencing (WGS), but the ASD studies utilizing WGS data in Chinese population are limited. In this study, we present a WGS study for 334 individuals, including 112 ASD patients and their non-ASD parents. We identified 146 de novo variants in coding regions in 85 cases and 60 inherited variants in coding regions. By integrating these variants with an association model, we identified 33 potential risk genes (P<0.001) enriched in neuron and regulation related biological process. Besides the well-known ASD genes (SCN2A, NF1, SHANK3, CHD8 etc.), several high confidence genes were highlighted by a series of functional analyses, including CTNND1, DGKZ, LRP1, DDN, ZNF483, NR4A2, SMAD6, INTS1, and MRPL12, with more supported evidence from GO enrichment, expression and network analysis. We also integrated RNA-seq data to analyze the effect of the variants on the gene expression and found 12 genes in the individuals with the related variants had relatively biased expression. We further presented the clinical phenotypes of the proband carrying the risk genes in both our samples and Caucasian samples to show the effect of the risk genes on phenotype. Regarding variants in non-coding regions, a total of 74 de novo variants and 30 inherited variants were predicted as pathogenic with high confidence, which were mapped to specific genes or regulatory features. The number of de novo variants found in patient was significantly associated with the parents' ages at the birth of the child, and gender with trend. We also identified small de novo structural variants in ASD trios. The results in this study provided important evidence for understanding the genetic mechanism of ASD.
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