ArticleNucleic acids research2020
Absence of MeCP2 binding to non-methylated GT-rich sequences in vivo.
Article in Nucleic acids research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- DNA methylation, nucleic acid structure, and rett mutations tune MeCP2 binding affinity and cooperativity.The Journal of biological chemistry · 2026Article
- MeCP2 requires interactions with nucleosome linker DNA to read chromatin DNA methylation.Nature communications · 2026Article
- Exploring the complexity of MECP2 function in Rett syndrome.Nature reviews. Neuroscience · 2025Review
- Interaction of methyl-CpG-binding protein 2 (MeCP2) with distinct enhancers in the mouse cortex.Nature neuroscience · 2025Article
- Downregulated SPESP1-driven fibroblast senescence decreases wound healing in aged mice.Clinical and translational medicine · 2024Article
- Extending MeCP2 interactome: canonical nucleosomal histones interact with MeCP2.Nucleic acids research · 2024Article
- A critique of the hypothesis that CA repeats are primary targets of neuronal MeCP2.Life science alliance · 2022Article
- Long-Term Treatment with Bortezomib Induces Specific Methylation Changes in Differentiated Neuronal Cells.Cancers · 2022Article
- Neuronal non-CG methylation is an essential target for MeCP2 function.Molecular cell · 2021Article
- The Molecular Functions of MeCP2 in Rett Syndrome Pathology.Frontiers in genetics · 2021Review
- Emerging Insights into the Distinctive Neuronal Methylome.Trends in genetics : TIG · 2020Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
MeCP2 is a nuclear protein that binds to sites of cytosine methylation in the genome. While most evidence confirms this epigenetic mark as the primary determinant of DNA binding, MeCP2 is also reported to have an affinity for non-methylated DNA sequences. Here we investigated the molecular basis and in vivo significance of its reported affinity for non-methylated GT-rich sequences. We confirmed this interaction with isolated domains of MeCP2 in vitro and defined a minimal target DNA sequence. Binding depends on pyrimidine 5' methyl groups provided by thymine and requires adjacent guanines and a correctly orientated A/T-rich flanking sequence. Unexpectedly, full-length MeCP2 protein failed to bind GT-rich sequences in vitro. To test for MeCP2 binding to these motifs in vivo, we analysed human neuronal cells using ChIP-seq and ATAC-seq technologies. While both methods robustly detected DNA methylation-dependent binding of MeCP2 to mCG and mCAC, neither showed evidence of MeCP2 binding to GT-rich motifs. The data suggest that GT binding is an in vitro phenomenon without in vivo relevance. Our findings argue that MeCP2 does not read unadorned DNA sequence and therefore support the notion that its primary role is to interpret epigenetic modifications of DNA.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.