ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Genomic landscape of transcriptional and epigenetic dysregulation in early onset polyglutamine disease.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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37 citing papers in PubMed, 73 citations in OpenAlex.
- Review
- Regulation of Genome Architecture in Huntington's Disease.Biochemistry · 2025Article
- Role of Calmodulin in Neurodegeneration and Neuroprotection.Mini reviews in medicinal chemistry · 2025Review
- The roles of TAF1 in neuroscience and beyond.Royal Society open science · 2024Review
- Brain-Derived Neurotrophic Factor Dysregulation as an Essential Pathological Feature in Huntington's Disease: Mechanisms and Potential Therapeutics.Biomedicines · 2023Review
- Transcriptional and Histone Acetylation Changes Associated with CRE Elements Expose Key Factors Governing the Regulatory Circuit in the Early Stage of Huntington's Disease Models.International journal of molecular sciences · 2023Article
- Polyglutamine-expanded ATXN7 alters a specific epigenetic signature underlying photoreceptor identity gene expression in SCA7 mouse retinopathy.Journal of biomedical science · 2022Article
- Acetylation State of Lysine 14 of Histone H3.3 Affects Mutant Huntingtin Induced Pathogenesis.International journal of molecular sciences · 2022Article
- 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
- Epigenetic regulation in Huntington's disease.Neurochemistry international · 2021Review
- Neuron type-specific increase in lamin B1 contributes to nuclear dysfunction in Huntington's disease.EMBO molecular medicine · 2021Article
- Age-related and disease locus-specific mechanisms contribute to early remodelling of chromatin structure in Huntington's disease mice.Nature communications · 2021Article
- How Do Post-Translational Modifications Influence the Pathomechanistic Landscape of Huntington's Disease? A Comprehensive Review.International journal of molecular sciences · 2020Review
- SVA insertion in X-linked Dystonia Parkinsonism alters histone H3 acetylation associated with TAF1 gene.PloS one · 2020Article
- Gene Deregulation and Underlying Mechanisms in Spinocerebellar Ataxias With Polyglutamine Expansion.Frontiers in neuroscience · 2020Review
- Transcriptional correlates of the pathological phenotype in a Huntington's disease mouse model.Scientific reports · 2019Article
- Epigenetic Regulation in Neurodegenerative Diseases.Trends in neurosciences · 2018Review
- The role of Twist1 in mutant huntingtin-induced transcriptional alterations and neurotoxicity.The Journal of biological chemistry · 2018Article
- Early alteration of epigenetic-related transcription in Huntington's disease mouse models.Scientific reports · 2018Article
- Comparison of spinocerebellar ataxia type 3 mouse models identifies early gain-of-function, cell-autonomous transcriptional changes in oligodendrocytes.Human molecular genetics · 2017Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transcriptional dysregulation is an important early feature of polyglutamine diseases. One of its proposed causes is defective neuronal histone acetylation, but important aspects of this hypothesis, such as the precise genomic topography of acetylation deficits and the relationship between transcriptional and acetylation alterations at the whole-genome level, remain unknown. The new techniques for the mapping of histone post-translational modifications at genomic scale enable such global analyses and are challenging some assumptions about the role of specific histone modifications in gene expression. We examined here the genome-wide correlation of histone acetylation and gene expression defects in a mouse model of early onset Huntington's disease. Our analyses identified hundreds of loci that were hypoacetylated for H3K9,14 and H4K12 in the chromatin of these mice. Surprisingly, few genes with altered transcript levels in mutant mice showed significant changes in these acetylation marks and vice versa. Our screen, however, identified a subset of genes in which H3K9,14 deacetylation and transcriptional dysregulation concur. Genes in this group were consistently affected in different brain areas, mouse models, and tissue from patients, which suggests a role in the etiology of this pathology. Overall, the combination of histone acetylation and gene expression screenings demonstrates that histone deacetylation and transcriptional dysregulation are two early, largely independent, manifestations of polyglutamine disease and suggests that additional epigenetic marks or mechanisms are required for explaining the full range of transcriptional alterations associated with this disorder.
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