ArticleScientific reports2017
Nucleocytoplasmic Shuttling of Histone Deacetylase 9 Controls Activity-Dependent Thalamocortical Axon Branching.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 17 citations in OpenAlex.
- Identification and validation of central amygdala FGFR1 as a therapeutic target for alcohol use disorder using single-nucleus sequencing in rats.Nature communications · 2026Article
- Decoding Epigenetic Switches: How Histone Acetylation/Deacetylation Regulates Mononuclear/Macrophage Fate in Bone Disorders.International journal of biological sciences · 2026Review
- Sensory modality-specific wiring of thalamocortical circuits.Nature reviews. Neuroscience · 2025Review
- Mapping the Interactions Among Class IIa Histone Deacetylases and Myocyte Enhancer Factor 2s.Journal of chemical information and modeling · 2025Article
- Epigenetic and Transcriptional Regulation of Spontaneous and Sensory Activity Dependent Programs During Neuronal Circuit Development.Frontiers in neural circuits · 2022Review
- Long-Lived Organotypic Slice Culture Model of the Rat Basolateral Amygdala.Current protocols · 2021Article
- TRANSPIRE: A Computational Pipeline to Elucidate Intracellular Protein Movements from Spatial Proteomics Data Sets.Journal of the American Society for Mass Spectrometry · 2020Article
- The class II histone deacetylases as therapeutic targets for Parkinson's disease.Neuronal signaling · 2020Review
- Class IIa HDACs regulate learning and memory through dynamic experience-dependent repression of transcription.Nature communications · 2019Article
- Location is everything: protein translocations as a viral infection strategy.Current opinion in chemical biology · 2019Review
- Regulation of Central Nervous System Development by Class I Histone Deacetylases.Developmental neuroscience · 2019Review
- Gene Co-expression Analysis Identifies Histone Deacetylase 5 and 9 Expression in Midbrain Dopamine Neurons and as Regulators of Neurite Growth via Bone Morphogenetic Protein Signaling.Frontiers in cell and developmental biology · 2019Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During development, thalamocortical (TC) axons form branches in an activity-dependent fashion. Here we investigated how neuronal activity is converted to molecular signals, focusing on an epigenetic mechanism involving histone deacetylases (HDACs). Immunohistochemistry demonstrated that HDAC9 was translocated from the nucleus to the cytoplasm of thalamic cells during the first postnatal week in rats. In organotypic co-cultures of the thalamus and cortex, fluorescent protein-tagged HDAC9 also exhibited nuclueocytoplasmic translocation in thalamic cells during culturing, which was reversed by tetrodotoxin treatment. Transfection with a mutant HDAC9 that interferes with the translocation markedly decreased TC axon branching in the culture. Similarly, TC axon branching was significantly decreased by the mutant HDAC9 gene transfer in vivo. However, axonal branching was restored by disrupting the interaction between HDAC9 and myocyte-specific enhancer factor 2 (MEF2). Taken together, the present results demonstrate that the nucleocytoplasmic translocation of HDAC9 plays a critical role in activity-dependent TC axon branching by affecting transcriptional regulation and downstream signaling pathways.
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