ArticleNeurobiology of disease2011
MeCP2 is required for global heterochromatic and nucleolar changes during activity-dependent neuronal maturation.
Article in Neurobiology of disease, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 76 citations in OpenAlex.
- MeCP2-driven chromatin organization controls nuclear stiffness.Communications biology · 2025Article
- Molecular Insights into Neurological Regression with a Focus on Rett Syndrome-A Narrative Review.International journal of molecular sciences · 2025Review
- DNA Methylation in Autism Spectrum Disorders: Biomarker or Pharmacological Target?Brain sciences · 2024Review
- Polymerase I as a Target for Treating Neurodegenerative Disorders.Biomedicines · 2024Review
- The Proteomic Composition and Organization of Constitutive Heterochromatin in Mouse Tissues.Cells · 2024Article
- Analysis of the interplay between MeCP2 and histone H1 duringEpigenetics · 2023Article
- Nuclear Architecture in the Nervous System.Results and problems in cell differentiation · 2022Review
- WGCNA Identifies Translational and Proteasome-Ubiquitin Dysfunction in Rett Syndrome.International journal of molecular sciences · 2021Article
- Nuclear Reorganization in Hippocampal Granule Cell Neurons from a Mouse Model of Down Syndrome: Changes in Chromatin Configuration, Nucleoli and Cajal Bodies.International journal of molecular sciences · 2021Article
- MeCP2 Levels Regulate the 3D Structure of Heterochromatic Foci in Mouse Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Order and disorder: abnormal 3D chromatin organization in human disease.Briefings in functional genomics · 2020Article
- AD7c-NTP Impairs Adult Striatal Neurogenesis by Affecting the Biological Function of MeCP2 in APP/PSl Transgenic Mouse Model of Alzheimer's Disease.Frontiers in aging neuroscience · 2020Article
- A genome-wide analysis reveals the MeCP2-dependent regulation of genes in BGC-823 cells.International journal of clinical and experimental pathology · 2020Article
- Genomic insights into MeCP2 function: A role for the maintenance of chromatin architecture.Current opinion in neurobiology · 2019Review
- MeCP2-E1 isoform is a dynamically expressed, weakly DNA-bound protein with different protein and DNA interactions compared to MeCP2-E2.Epigenetics & chromatin · 2019Article
- MeCP2: A Critical Regulator of Chromatin in Neurodevelopment and Adult Brain Function.International journal of molecular sciences · 2019Review
- Understanding intellectual disability and autism spectrum disorders from common mouse models: synapses to behaviour.Open biology · 2019Review
- Ribosomal biogenesis as an emerging target of neurodevelopmental pathologies.Journal of neurochemistry · 2019Review
- The effects of biological aging on global DNA methylation, histone modification, and epigenetic modifiers in the mouse germinal vesicle stage oocyte.Animal reproduction · 2018Article
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7 authors at 1 institution in 1 country.
Funding
Abstract
Mutations in MECP2, encoding methyl CpG binding protein 2, cause the neurodevelopmental disorder Rett syndrome. MeCP2 is an abundant nuclear protein that binds to chromatin and modulates transcription in response to neuronal activity. Prior studies of MeCP2 function have focused on specific gene targets of MeCP2, but a more global role for MeCP2 in neuronal nuclear maturation has remained unexplored. MeCP2 levels increase during postnatal brain development, coinciding with dynamic changes in neuronal chromatin architecture, particularly detectable as changes in size, number, and location of nucleoli and perinucleolar heterochromatic chromocenters. To determine a potential role for MeCP2 in neuronal chromatin maturational changes, we measured nucleoli and chromocenters in developing wild-type and Mecp2-deficient mouse cortical sections, as well as mouse primary cortical neurons and a human neuronal cell line following induced maturation. Mecp2-deficient mouse neurons exhibited significant differences in nucleolar and chromocenter number and size, as more abundant, smaller nucleoli in brain and primary neurons compared to wild-type, consistent with delayed neuronal nuclear maturation in the absence of MeCP2. Primary neurons increased chromocenter size following depolarization in wild-type, but not Mecp2-deficient cultures. Wild-type MECP2e1 over-expression in human SH-SY5Y cells was sufficient to induce significantly larger nucleoli, but not a T158M mutation of the methyl-binding domain. These results suggest that, in addition to the established role of MeCP2 in transcriptional regulation of specific target genes, the global chromatin-binding function of MeCP2 is essential for activity-dependent global chromatin dynamics during postnatal neuronal maturation.
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