ArticleMolecular psychiatry2021
AUTS2 isoforms control neuronal differentiation.
Article in Molecular psychiatry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 56 citations in OpenAlex.
- Single-nucleus atlas of cell-type specific genetic regulation in the human brain.Nature genetics · 2026Article
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- BRD1 haploinsufficiency alters early neuronal programming and disrupts maturation in human induced glutamatergic neurons.Research square · 2026Article
- Fbrsl1 is required for cranial neural crest development and reflects a conserved function of the human disease-associated protein.Disease models & mechanisms · 2025Article
- Research on the potential mechanisms and therapeutic drug for the co-occurrence of major depressive disorder in castration-resistant prostate cancer.Scientific reports · 2025Article
- FBRSL1 regulates the expression of chromatin regulators BRPF1 and KAT6A.Human genetics · 2025Article
- Auts2 enhances neurogenesis and promotes expansion of the cerebral cortex.Journal of advanced research · 2025Article
- Parent-of-origin regulation by maternal auts2 shapes neurodevelopment and behavior in fish.Genome biology · 2025Article
- The microcephaly-associated transcriptional regulator AUTS2 cooperates with Polycomb complex PRC2 to produce upper-layer neurons in mice.The EMBO journal · 2025Article
- AUTS2 disruption causes neuronal differentiation defects in human cerebral organoids through hyperactivation of the WNT/β-catenin pathway.Scientific reports · 2024Article
- H2A monoubiquitination: insights from human genetics and animal models.Human genetics · 2024Review
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- Silencing of theFrontiers in pharmacology · 2024Article
- Activity-Dependent Differential Regulation of Auts2 Isoforms In Vitro and In Vivo.Molecular neurobiology · 2023Article
- An O-GlcNAc transferase pathogenic variant linked to intellectual disability affects pluripotent stem cell self-renewal.Disease models & mechanisms · 2023Article
- Structural polymorphism driven by a register shift in a CGAG-rich region found in the promoter of the neurodevelopmental regulator AUTS2 gene.Nucleic acids research · 2023Article
- Investigation of autism-related transcription factors underlying sex differences in the effects of bisphenol A on transcriptome profiles and synaptogenesis in the offspring hippocampus.Biology of sex differences · 2023Article
- AUTS2 Controls Neuronal Lineage Choice Through a Novel PRC1-Independent Complex and BMP Inhibition.Stem cell reviews and reports · 2023Article
- Cerebral organoids containing an AUTS2 missense variant model microcephaly.Brain : a journal of neurology · 2023Article
- Review
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in AUTS2 are associated with autism, intellectual disability, and microcephaly. AUTS2 is expressed in the brain and interacts with polycomb proteins, yet it is still unclear how mutations in AUTS2 lead to neurodevelopmental phenotypes. Here we report that when neuronal differentiation is initiated, there is a shift in expression from a long isoform to a short AUTS2 isoform. Yeast two-hybrid screen identified the splicing factor SF3B1 as an interactor of both isoforms, whereas the polycomb group proteins, PCGF3 and PCGF5, were found to interact exclusively with the long AUTS2 isoform. Reporter assays showed that the first exons of the long AUTS2 isoform function as a transcription repressor, but the part that consist of the short isoform acts as a transcriptional activator, both influenced by the cellular context. The expression levels of PCGF3 influenced the ability of the long AUTS2 isoform to activate or repress transcription. Mouse embryonic stem cells (mESCs) with heterozygote mutations in Auts2 had an increase in cell death during in vitro corticogenesis, which was significantly rescued by overexpressing the human AUTS2 transcripts. mESCs with a truncated AUTS2 protein (missing exons 12-20) showed premature neuronal differentiation, whereas cells overexpressing AUTS2, especially the long transcript, showed increase in expression of pluripotency markers and delayed differentiation. Taken together, our data suggest that the precise expression of AUTS2 isoforms is essential for regulating transcription and the timing of neuronal differentiation.
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