ArticleNature communications2026
MeCP2 requires interactions with nucleosome linker DNA to read chromatin DNA methylation.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed.
- Clinical Epigenomics in Rare Diseases: Interpreting DNA Methylation Episignatures.Molecular genetics & genomic medicine · 2026Review
- Gene regulatory mechanisms downstream of DNA methylation.Nature reviews. Genetics · 2026Review
- The implications of TMSB4X in TIM3 hypermethylation and CD8Scientific reports · 2026Article
- MeCP2 functions as a DNA methylation reader in immune homeostasis and cancer.Frontiers in epigenetics and epigenomics · 2026Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Methyl-CpG-binding protein 2 (MeCP2) is a clinically important epigenetic reader that is essential for neuronal function, but how it binds methylated DNA within the protein-DNA complexes that comprise chromatin is unclear. Using designer nucleosomes, we observe that MeCP2 is able to engage methylated DNA at multiple sites on the nucleosome surface. Surprisingly, even methyl-cytosine placed in bent, histone-contacting, core nucleosomal DNA can be bound. However, we find that this ability requires interactions with inter-nucleosomal linker DNA. Nucleosome core DNA methylation reading involves regions of MeCP2 beyond its canonical methyl-CpG binding domain and we define a novel DNA-binding region in MeCP2 that is required for this function. We further demonstrate that histone H1 antagonises the MeCP2-nucleosome interactions by competing for linker DNA. Overall, our study reveals that MeCP2 gains access to methylated chromatinised DNA, independent of nucleosome structure, via essential nonspecific interactions with linker DNA.
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