ArticleNature neuroscience2023
Non-synaptic function of the autism spectrum disorder-associated gene SYNGAP1 in cortical neurogenesis.
Article in Nature neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 78 citations in OpenAlex.
- Pathological Priming and Developmental Heterochrony as Organizing Concepts in Human iPSC Models of Autism Spectrum Disorder.Molecular neurobiology · 2026Review
- Natural medicine‑empowered treatment of depression via restoring neurogenesis (Review).Molecular medicine reports · 2026Review
- Elucidating the role of DEAF1 in neurodevelopment and shared molecular pathways in high-risk autism genes using cortical organoids.Science advances · 2026Article
- Genetic Rescue of Disrupted Synaptic Protein Interaction Network Dynamics Following SYNGAP1 Reactivation.Molecular & cellular proteomics : MCP · 2026Article
- Generation, differentiation, and potential of three radial glial subtypes in human cortical organoids.BMB reports · 2026Review
- Advances and applications of brain organoids in central nervous system disorders: Bridging the gap from laboratory to clinic.Neural regeneration research · 2026Article
- The Synaptic Clock: SynGAP1 as a Molecular Timer of Postsynaptic Density Consolidation.Biomolecules · 2026Review
- Spatially defined axonal guidance in neural organoids with micropatterned microfluidic channels.bioRxiv : the preprint server for biology · 2026Article
- Transcriptomic and phenotypic convergence of neurodevelopmental disorder risk genes in vitro and in vivo.Nature neuroscience · 2026Article
- FABP7 controls radial glial scaffold stability during human cortical development.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Resolving Diagnostic Uncertainty in Neurodevelopmental Disorders Using Exome Sequencing Supported by Literature-Based Multi-Omics Evidence.Biomolecules · 2026Article
- Disruption of the SYNGAP1 PDZ ligand motif accelerates differentiation of human iPSC-derived GABAergic neurons.bioRxiv : the preprint server for biology · 2026Article
- Splice isoform-perturbation coupled to single cell transcriptome profiling reveals functions of microexons in neurogenesis and autism-linked pathways.Nature communications · 2026Article
- Using the linear references from the pangenome to discover missing autism variants.Nature communications · 2026Article
- Preconfigured neuronal firing sequences in human brain organoids.Nature neuroscience · 2026Article
- Article
- Pluripotent stem cells-based neural organoids for modelling human brain development and diseases.Cell & bioscience · 2025Review
- MeCP2 regulates telencephalic development in human cerebral organoids.Cell reports · 2025Article
- Syngap1 and the development of murine neocortical progenitor cells.Nature communications · 2025Article
- Genetic rescue of disrupted synaptic protein interaction network dynamics followingbioRxiv : the preprint server for biology · 2025Article
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Authors and funding
20 authors at 6 institutions in 2 countries.
Funding
Abstract
Genes involved in synaptic function are enriched among those with autism spectrum disorder (ASD)-associated rare genetic variants. Dysregulated cortical neurogenesis has been implicated as a convergent mechanism in ASD pathophysiology, yet it remains unknown how 'synaptic' ASD risk genes contribute to these phenotypes, which arise before synaptogenesis. Here, we show that the synaptic Ras GTPase-activating (RASGAP) protein 1 (SYNGAP1, a top ASD risk gene) is expressed within the apical domain of human radial glia cells (hRGCs). In a human cortical organoid model of SYNGAP1 haploinsufficiency, we find dysregulated cytoskeletal dynamics that impair the scaffolding and division plane of hRGCs, resulting in disrupted lamination and accelerated maturation of cortical projection neurons. Additionally, we confirmed an imbalance in the ratio of progenitors to neurons in a mouse model of Syngap1 haploinsufficiency. Thus, SYNGAP1-related brain disorders may arise through non-synaptic mechanisms, highlighting the need to study genes associated with neurodevelopmental disorders (NDDs) in diverse human cell types and developmental stages.
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