ArticleMolecular psychiatry2019
Disruption of TCF4 regulatory networks leads to abnormal cortical development and mental disabilities.
Article in Molecular psychiatry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.
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Who cites it
57 citing papers in PubMed, 1 synthesis or guideline pooled it, 102 citations in OpenAlex.
- Adult brain neurons require continual expression of the schizophrenia-risk gene Tcf4 for structural and functional integrity.Translational psychiatry · 2021Pooled it
- Developmental and cellular vulnerabilities underlie genetic architecture of schizophrenia.Molecular psychiatry · 2026Article
- Myelin, white matter, and social deficits in autism spectrum disorder.Neural regeneration research · 2026Article
- Identification and prioritization of gene sets associated with schizophrenia risk by network analysis.Psychopharmacology · 2026Article
- Article
- Selective enrichment of TCF4 in GABAergic neurons during postnatal primate development.Frontiers in neuroanatomy · 2026Article
- Juvenile reinstatement of TCF4 in Pitt-Hopkins syndrome model mice reveals a critical window for genetic intervention.bioRxiv : the preprint server for biology · 2025Article
- Tcf4 Deficiency causes recurrent seizures in mice.Progress in neurobiology · 2025Article
- Transcriptomic insights into fate choice of pallial versus subpallial GABAergic neurons.Nature communications · 2025Article
- Implementation of the Methyl-Seq platform to identify tissue- and sex-specific DNA methylation differences in the rat epigenome.Epigenetics · 2024Article
- Recruitment of homodimeric proneural factors by conserved CAT-CAT E-boxes drives major epigenetic reconfiguration in cortical neurogenesis.Nucleic acids research · 2024Article
- PONYTA: prioritization of phenotype-related genes from mouse KO events using PU learning on a biological network.Bioinformatics (Oxford, England) · 2024Article
- Astrocyte allocation during brain development is controlled by Tcf4-mediated fate restriction.The EMBO journal · 2024Article
- TCF4 Mutations Disrupt Synaptic Function Through Dysregulation of RIMBP2 in Patient-Derived Cortical Neurons.Biological psychiatry · 2024Article
- Mendelian randomization and single-cell expression analyses identify the causal relationship between depression and chronic rhinosinusitis.Frontiers in psychiatry · 2024Article
- Transcription factor 4 expression in the developing non-human primate brain: a comparative analysis with the mouse brain.Frontiers in neuroanatomy · 2024Article
- MicroRNA-495 Modulates Neuronal Layer Fate Determination by TargetingInternational journal of biological sciences · 2024Article
- Psychiatric risk gene Transcription Factor 4 (TCF4) regulates the density and connectivity of distinct inhibitory interneuron subtypes.Molecular psychiatry · 2023Article
- Distinct requirements for Tcf3 and Tcf12 during oligodendrocyte development in the mouse telencephalon.Neural development · 2023Article
- Brain-specific Pd1 deficiency leads to cortical neurogenesis defects and depressive-like behaviors in mice.Cell death and differentiation · 2023Article
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
Abstract
The TCF4 gene is the subject of numerous and varied investigations of it's role in the genesis of neuropsychiatric disease. The gene has been identified as the cause of Pitt-Hopkins syndrome (PTHS) and it has been implicated in various other neuropsychiatric diseases, including schizophrenia, depression, and autism. However, the precise molecular mechanisms of the gene's involvement in neurogenesis, particularly, corticogenesis, are not well understood. Here, we present data showing that TCF4 is expressed in a region-specific manner in the radial glia and stem cells of transient embryonic zones at early gestational ages in both humans and mice. TCF4 haploinsufficiency mice exhibit a delay in neuronal migration, and a significant increase in the number of upper-layer cortical neurons, as well as abnormal dendrite and synapse formation. Our research also reveals that TCF3 up-regulates Tcf4 by binding to the specific "E-box" and its flank sequence in intron 2 of the Tcf4 gene. Additionally, our transcriptome study substantiates that Tcf4 transcriptional function is essential for locomotion, cognition, and learning. By activating expression of TCF4 in the regulation of neuronal proliferation and migration to the overlaying neocortex and subsequent differentiation leading to laminar formation TCF4 fulfills its normal function, but if not, abnormalities such as those reported here result. These findings provide new insight into the specific roles of Tcf4 molecular pathway in neocortical development and their relevance in the pathogenesis of neuropsychiatric diseases.
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