ArticleNature communications2020
KAT3-dependent acetylation of cell type-specific genes maintains neuronal identity in the adult mouse brain.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 48 citations in OpenAlex.
- Neurogenesis and the Epigenetic Landscape: Role of Histone Modifications and Chromatin Remodeling.Brain and behavior · 2026Review
- Photoperiod-driven gene regulation in the brain ofFrontiers in endocrinology · 2026Article
- Cell type-specific functions of the PBAF chromatin-remodeling complex in neuronal diversification.Nature communications · 2025Article
- Neuronal type-specific modulation of cognition and AP-1 signaling by early-life rearing conditions.Nature communications · 2025Article
- Genetic Mechanisms of Experience-Dependent Neuronal Plasticity.Annual review of genetics · 2025Review
- Sex-specific modulation of anxiety-like behavior by forebrain neuronal SMC3 in mice.Translational psychiatry · 2025Article
- A rapid chemical reprogramming system to generate human pluripotent stem cells.Nature chemical biology · 2025Article
- Transcriptome and acetylome profiling identify crucial steps of neuronal differentiation in Rubinstein-Taybi syndrome.Communications biology · 2024Article
- EnhancerNet: a predictive model of cell identity dynamics through enhancer selection.Development (Cambridge, England) · 2024Article
- Lactylation: A Novel Post-Translational Modification with Clinical Implications in CNS Diseases.Biomolecules · 2024Review
- Targeting neuronal epigenomes for brain rejuvenation.The EMBO journal · 2024Review
- Single cell tracing of Pomc neurons reveals recruitment of 'Ghost' subtypes with atypical identity in a mouse model of obesity.Nature communications · 2024Article
- Kdm1a safeguards the topological boundaries of PRC2-repressed genes and prevents aging-related euchromatinization in neurons.Nature communications · 2024Article
- Maintenance of neuronal identity in C. elegans and beyond: Lessons from transcription and chromatin factors.Seminars in cell & developmental biology · 2024Review
- Balanced SET levels favor the correct enhancer repertoire during cell fate acquisition.Nature communications · 2023Article
- Polyglutamine-expanded ATXN7 alters a specific epigenetic signature underlying photoreceptor identity gene expression in SCA7 mouse retinopathy.Journal of biomedical science · 2022Article
- Article
- CBP Is Required for Establishing Adaptive Gene Programs in the Adult Mouse Brain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Activity-Induced Cortical Glutamatergic Neuron Nascent Proteins.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Multiomic Analysis of Neurons with Divergent Projection Patterns Identifies Novel Regulators of Axon Pathfinding.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The lysine acetyltransferases type 3 (KAT3) family members CBP and p300 are important transcriptional co-activators, but their specific functions in adult post-mitotic neurons remain unclear. Here, we show that the combined elimination of both proteins in forebrain excitatory neurons of adult mice resulted in a rapidly progressing neurological phenotype associated with severe ataxia, dendritic retraction and reduced electrical activity. At the molecular level, we observed the downregulation of neuronal genes, as well as decreased H3K27 acetylation and pro-neural transcription factor binding at the promoters and enhancers of canonical neuronal genes. The combined deletion of CBP and p300 in hippocampal neurons resulted in the rapid loss of neuronal molecular identity without de- or transdifferentiation. Restoring CBP expression or lysine acetylation rescued neuronal-specific transcription in cultured neurons. Together, these experiments show that KAT3 proteins maintain the excitatory neuron identity through the regulation of histone acetylation at cell type-specific promoter and enhancer regions.
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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.