ArticleNucleic acids research2018
Brain-specific deletion of histone variant H2A.z results in cortical neurogenesis defects and neurodevelopmental disorder.
Article in Nucleic acids research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 81 citations in OpenAlex.
- Spatially resolved mapping of histones reveals selective neuronal response in Rett syndrome.The FEBS journal · 2026Article
- Convergent genetic pathways linking neuropsychiatric and ocular disorders in children.Journal of child psychology and psychiatry, and allied disciplines · 2026Article
- Mechanisms of gene regulation by SRCAP and H2A.Z.Nature communications · 2026Article
- Acetate enhances long-term memory in female mice by sex-, context-, and brain region-specific epigenetic and transcriptional remodeling.Science signaling · 2026Article
- Skin Epidermal Progenitor Maintenance by the SRCAP-H2A.Z Axis Downstream to Extracellular Signal-Regulated Kinase and mTOR Signaling.The Journal of investigative dermatology · 2026Article
- Translational biomarkers of hypoxic brain injury uncovered in CSF secreting human choroid plexus organoids.Fluids and barriers of the CNS · 2025Article
- Analysis of Genomic and Transcriptomic Data Revealed Key Genes and Processes in the Development of Major Depressive Disorder.International journal of molecular sciences · 2025Article
- Environmental Xenobiotics and Epigenetic Modifications: Implications for Human Health and Disease.Journal of xenobiotics · 2025Review
- Unraveling Neurodevelopment: Synergistic Effects of Intrinsic Genetic Programs and Extrinsic Environmental Cues.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Histone variants: expanding the epigenetic potential of neurons one amino acid at a time.Trends in biochemical sciences · 2025Review
- Elucidating neuroepigenetic mechanisms to inform targeted therapeutics for brain disorders.iScience · 2025Review
- Multifunctional histone variants in genome function.Nature reviews. Genetics · 2025Review
- The Function of H2A Histone Variants and Their Roles in Diseases.Biomolecules · 2024Review
- A multiomic atlas of the aging hippocampus reveals molecular changes in response to environmental enrichment.Nature communications · 2024Article
- Role of the histone variant H2A.Z.1 in memory, transcription, and alternative splicing is mediated by lysine modification.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024Article
- Histone H1x in mouse ventral hippocampus associates with, but does not cause behavioral adaptations to stress.Translational psychiatry · 2024Article
- Behavioral and transcriptional effects of repeated electroconvulsive seizures in the neonatal MK-801-treated rat model of schizophrenia.Psychopharmacology · 2024Article
- Roles of Histone H2A Variants in Cancer Development, Prognosis, and Treatment.International journal of molecular sciences · 2024Review
- The Dynamics of Histone Modifications during Mammalian Zygotic Genome Activation.International journal of molecular sciences · 2024Review
- Control of Intestinal Stemness and Cell Lineage by Histone Variant H2A.Z Isoforms.Molecular and cellular biology · 2024Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Defects in neurogenesis alter brain circuit formations and may lead to neurodevelopmental disorders such as autism and schizophrenia. Histone H2A.z, a variant of histone H2A, plays critical roles in chromatin structure and epigenetic regulation, but its function and mechanism in brain development remain largely unknown. Here, we find that the deletion of H2A.z results in enhanced proliferation of neural progenitors but reduced neuronal differentiation. In addition, neurons in H2A.z knockout mice exhibit abnormal dendrites during brain development. Furthermore, H2A.zcKO mice exhibit serial behavioral deficits, such as decreased exploratory activity and impaired learning and memory. Mechanistically, H2A.z regulates embryonic neurogenesis by targeting Nkx2-4 through interaction with Setd2, thereby promoting H3K36me3 modification to activate the transcription of Nkx2-4. Furthermore, enforced expression of Nkx2-4 can rescue the defective neurogenesis in the H2A.z-knockdown embryonic brain. Together, our findings implicate the epigenetic regulation by H2A.z in embryonic neurogenesis and provide a framework for understanding how disruption in the H2A.z gene may contribute to neurological disorders.
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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.