DNA Methylation-Related Chromatin Remodeling in Activity-Dependent Bdnf Gene Regulation
Abstract
In conjunction with histone modifications, DNA methylation plays critical roles in gene silencing through chromatin remodeling. Changes in DNA methylation perturb neuronal function, and mutations in a methyl-CpG–binding protein, MeCP2, are associated with Rett syndrome. We report that increased synthesis of brain-derived neurotrophic factor (BDNF) in neurons after depolarization correlates with a decrease in CpG methylation within the regulatory region of the Bdnf gene. Moreover, increased Bdnf transcription involves dissociation of the MeCP2–histone deacetylase–mSin3A repression complex from its promoter. Our findings suggest that DNA methylation–related chromatin remodeling is important for activity-dependent gene regulation that may be critical for neural plasticity.
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Increased CpG methylation in the promoter region of the BDNF gene correlates with decreased BDNF synthesis in neurons.
“increased CpG methylation in the promoter region of the gene encoding brain-derived neurotrophic factor (BDNF) has been found to correlate with a decreased synthesis of BDNF in neurons.53”
From Epigenetic regulation in major depression and other stress-related disorders: molecular mechanisms, clinical relevance and therapeutic potential (2023) · cites this paper as [53]
MeCP2 acts as a bridge between DNA methylation marks and HDACs, enzymes involved in histone modifications.
“MeCP2 is known to act as a bridge between DNA methylation marks and HDACs, enzymes involved in histone modifications and has been shown to dock at CpG-methylated sites and recruit HDACs to the chromatin, forming a silencing complex that represses gene transcription (Martinowich et al., 2003).”
From The Epigenetics of Anxiety Pathophysiology: A DNA Methylation and Histone Modification Focused Review (2023) · cites this paper as Martinowich et al., 2003
MeCP2 binding to chromatin is partially impaired if CpG sites are hypomethylated.
“This binding is partially impaired if CpG sites are hypomethylated (Martinowich et al., 2003).”
From The Epigenetics of Anxiety Pathophysiology: A DNA Methylation and Histone Modification Focused Review (2023) · cites this paper as Martinowich et al., 2003
MeCP2 docks at CpG-methylated sites and recruits HDACs to the chromatin, forming a silencing complex that represses gene transcription.
“MeCP2 is known to act as a bridge between DNA methylation marks and HDACs, enzymes involved in histone modifications and has been shown to dock at CpG-methylated sites and recruit HDACs to the chromatin, forming a silencing complex that represses gene transcription (Martinowich et al., 2003).”
From The Epigenetics of Anxiety Pathophysiology: A DNA Methylation and Histone Modification Focused Review (2023) · cites this paper as Martinowich et al., 2003
Following depolarization of mouse embryonic day 15 (E14) cortical cells, MeCP2 was partially dissociated from the Bdnf promoter.
“Following depolarization of mouse embryonic day 15 (E14) cortical cells, MeCP2 was found to be partially dissociated from the Bdnf promoter, suggesting that neuronal firing may redistribute MeCP2 binding allowing for BDNF expression (Martinowich et al., 2003).”
From The Epigenetics of Anxiety Pathophysiology: A DNA Methylation and Histone Modification Focused Review (2023) · cites this paper as Martinowich et al., 2003
Neuronal firing may redistribute MeCP2 binding allowing for BDNF expression.
“Following depolarization of mouse embryonic day 15 (E14) cortical cells, MeCP2 was found to be partially dissociated from the Bdnf promoter, suggesting that neuronal firing may redistribute MeCP2 binding allowing for BDNF expression (Martinowich et al., 2003).”
From The Epigenetics of Anxiety Pathophysiology: A DNA Methylation and Histone Modification Focused Review (2023) · cites this paper as Martinowich et al., 2003
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- Authors
- Martinowich, K., Hattori, D., Wu, H., Fouse, S., He, F., Hu, Y., Fan, G., & Sun, Y. E.
- Affiliations
- University of California, Los Angeles (US)
- Corresponding author
- Hattori, Daisuke
- Wu, Hao
- Fouse, Shaun
- Fan, Guoping
- Sun, Yi E.
- Venue
- Science
- Published
- 2003-10-31
- Volume
- 302
- Issue
- 5646
- Pages
- 890-893
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W2067004457
- Cited by
- 1,405
- References
- 28
- Citations by year
- 2026: 23 · 2025: 31 · 2024: 28 · 2023: 27 · 2022: 47 · 2021: 81 · 2020: 47 · 2019: 36 · 2018: 49 · 2017: 88 · 2016: 73 · 2015: 76 · 2014: 99 · 2013: 86 · 2012: 102
- FWCI
- 18.01
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- The HKU Scholars Hub (University of Hong Kong) (submittedVersion)
- Funders
- National Institute of Neurological Disorders and Stroke (NS-44405, R01NS044405)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Keywords
- DNA methylation, chromatin remodeling, brain-derived neurotrophic factor, MeCP2, histone deacetylase, mSin3A, CpG methylation, neuronal depolarization, activity-dependent gene expression, neuroplasticity, Rett syndrome, gene silencing
- MeSH terms
- Animals, Cells, Cultured, Chromatin, Chromosomal Proteins, Non-Histone, DNA-Binding Proteins, Gene Expression Regulation, Histone Deacetylases, Mice, Inbred BALB C, Models, Genetic, Neuronal Plasticity, Neurons, Potassium Chloride, Promoter Regions, Genetic, Repressor Proteins, Transcription Factors, Transcription, Genetic, Transfection, Cyclic AMP Response Element-Binding Protein, CpG Islands, DNA Methylation, Brain-Derived Neurotrophic Factor, Response Elements, Gene Silencing, Mice, Methyl-CpG-Binding Protein 2, Sin3 Histone Deacetylase and Corepressor Complex
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