ArticleNucleic acids research2023
DNA strand asymmetry generated by CpG hemimethylation has opposing effects on CTCF binding.
Article in Nucleic acids research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Roles of transposable elements and DNA methylation in the formation of CpG islands and CpG-depleted regulatory elements.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Dam-dependent epigenetic memory regulates prophage reintegration in Salmonella.Nucleic acids research · 2025Article
- Double and single stranded detection of 5-methylcytosine and 5-hydroxymethylcytosine with nanopore sequencing.Communications biology · 2025Article
- Epigenomic heterogeneity as a source of tumour evolution.Nature reviews. Cancer · 2025Review
- DNA-binding proteins from MBD through ZF to BEN: recognition of cytosine methylation status by one arginine with two conformations.Nucleic acids research · 2024Article
- Machine learning enables pan-cancer identification of mutational hotspots at persistent CTCF binding sites.Nucleic acids research · 2024Article
- Tumor detection by analysis of both symmetric- and hemi-methylation of plasma cell-free DNA.Nature communications · 2024Article
- Article
- Uncovering the roles of DNA hemi-methylation in transcriptional regulation using MspJI-assisted hemi-methylation sequencing.Nucleic acids research · 2024Article
- Structures of CTCF-DNA complexes including all 11 zinc fingers.Nucleic acids research · 2023Article
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Authors and funding
8 authors.
Funding
Abstract
CpG methylation generally occurs on both DNA strands and is essential for mammalian development and differentiation. Until recently, hemimethylation, in which only one strand is methylated, was considered to be simply a transitory state generated during DNA synthesis. The discovery that a subset of CCCTC-binding factor (CTCF) binding sites is heritably hemimethylated suggests that hemimethylation might have an unknown biological function. Here we show that the binding of CTCF is profoundly altered by which DNA strand is methylated and by the specific CTCF binding motif. CpG methylation on the motif strand can inhibit CTCF binding by up to 7-fold, whereas methylation on the opposite strand can stimulate binding by up to 4-fold. Thus, hemimethylation can alter binding by up to 28-fold in a strand-specific manner. The mechanism for sensing methylation on the opposite strand requires two critical residues, V454 and S364, within CTCF zinc fingers 7 and 4. Similar to methylation, CpG hydroxymethylation on the motif strand can inhibit CTCF binding by up to 4-fold. However, hydroxymethylation on the opposite strand removes the stimulatory effect. Strand-specific methylation states may therefore provide a mechanism to explain the transient and dynamic nature of CTCF-mediated chromatin interactions.
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