Cited by 567RNA Research and SplicingEpigenetics and DNA MethylationGenomics and Chromatin Dynamics

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Intragenic DNA methylation modulates alternative splicing by recruiting MeCP2 to promote exon recognition

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Maunakea, Alika K, Chepelev, Iouri, Cui, Kairong, Zhao, Keji·2013·Cell Research

DOI 10.1038/cr.2013.110PMC PMC3817542

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Abstract

Although the function of DNA methylation in gene promoter regions is well established in transcriptional repression, the function of the evolutionarily conserved widespread distribution of DNA methylation in gene body regions remains incompletely understood. Here, we show that DNA methylation is enriched in included alternatively spliced exons (ASEs), and that inhibition of DNA methylation results in aberrant splicing of ASEs. The methyl-CpG-binding protein MeCP2 is enriched in included ASEs, particularly those that are also highly methylated, and inhibition of DNA methylation disrupts specific targeting of MeCP2 to exons. Interestingly, ablation of MeCP2 results in increased histone acetylation and aberrant ASE-skipping events. We further show that inhibition of histone deacetylase (HDAC) activity leads to exon skipping that shows a highly significant degree of overlap with that caused by MeCP2 knockdown. Together, our data indicate that intragenic DNA methylation operates in exon definition to modulate alternative RNA splicing and can enhance exon recognition via recruitment of the multifunctional protein MeCP2, which thereby maintains local histone hypoacetylation through the subsequent recruitment of HDACs.

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Additional file 4 of Combined single-cell profiling of expression and DNA methylation reveals splicing regulation and heterogeneity
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Additional file 5 of A variability in response of osteoclasts to zoledronic acid is mediated by smoking-associated modification in the DNA methylome
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Additional file 7 of A variability in response of osteoclasts to zoledronic acid is mediated by smoking-associated modification in the DNA methylome
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Additional file 2 of Combined single-cell profiling of expression and DNA methylation reveals splicing regulation and heterogeneity
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Additional file 1 of Combined single-cell profiling of expression and DNA methylation reveals splicing regulation and heterogeneity
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Additional file 10 of Combined single-cell profiling of expression and DNA methylation reveals splicing regulation and heterogeneity
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Additional file 8 of Combined single-cell profiling of expression and DNA methylation reveals splicing regulation and heterogeneity
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Additional file 3 of A variability in response of osteoclasts to zoledronic acid is mediated by smoking-associated modification in the DNA methylome
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Additional file 6 of Combined single-cell profiling of expression and DNA methylation reveals splicing regulation and heterogeneity
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Additional file 9 of Combined single-cell profiling of expression and DNA methylation reveals splicing regulation and heterogeneity
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Additional file 5 of Combined single-cell profiling of expression and DNA methylation reveals splicing regulation and heterogeneity
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Additional file 6 of A variability in response of osteoclasts to zoledronic acid is mediated by smoking-associated modification in the DNA methylome
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Additional file 7 of Combined single-cell profiling of expression and DNA methylation reveals splicing regulation and heterogeneity
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Additional file 3 of Shifts in the immunoepigenomic landscape of monocytes in response to a diabetes-specific social support intervention: a pilot study among Native Hawaiian adults with diabetes
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Additional file 2 of Shifts in the immunoepigenomic landscape of monocytes in response to a diabetes-specific social support intervention: a pilot study among Native Hawaiian adults with diabetes
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Authors: Maunakea, A. K., Chepelev, I., Cui, K., & Zhao, K.
Affiliations: University of Hawaiʻi at Mānoa (US)
Cincinnati Children's Hospital Medical Center (US)
National Institutes of Health (US)
Corresponding author: Zhao, Keji
ORCID: Maunakea, Alika K
Chepelev, Iouri
Zhao, Keji
Venue: Cell Research
Publisher: Springer Science and Business Media LLC
Published: 2013-08-13
Volume: 23
Issue: 11
Pages: 1256-1269
ISSN: 1001-0602 (ISSN-L)
1748-7838
DOI: 10.1038/cr.2013.110
PMC: PMC3817542
OpenAlex: W2074898309
Cited by: 552
References: 46
Citations by year: 2026: 17 · 2025: 19 · 2024: 26 · 2023: 32 · 2022: 32 · 2021: 55 · 2020: 47 · 2019: 57 · 2018: 42 · 2017: 57 · 2016: 59 · 2015: 53 · 2014: 48 · 2013: 6
FWCI: 24.77
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by-nc-nd
creativecommons.org/licenses/by-nc-nd/3.0/ (tdm)
Locations: Cell Research (publishedVersion, cc-by-nc-nd)
Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
PubMed Central (publishedVersion, cc-by-nc-nd)
PubMed (publishedVersion)
Funders: Johns Hopkins University (HCT116)
National Institutes of Health
University of California, San Francisco
National Heart, Lung, and Blood Institute
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA Research and Splicing
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
Keywords: alternative splicing, MeCP2, exon skipping, exon recognition, histone acetylation, histone deacetylase, gene body methylation, methyl-CpG binding proteins, RNA splicing regulation
MeSH terms: Cell Line, Exons, Humans, Alternative Splicing, DNA Methylation, HCT116 Cells, Methyl-CpG-Binding Protein 2

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Intragenic DNA methylation modulates alternative splicing by recruiting MeCP2 to promote exon recognition

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