ArticleNucleic acids research2025
CTCF binding landscape is shaped by the epigenetic state of the N-terminal nucleosome in relation to CTCF motif orientation.
Article in Nucleic acids research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Intrinsic DNA codes govern distinct modes of nucleosome-transcription factor interactions.Nature communications · 2026Article
- Histone H4 acetyl-methyllysine marks accessible chromatin that resists compaction.bioRxiv : the preprint server for biology · 2026Article
- Therapy-associated mutagenesis at CTCF binding sites is shaped by chromatin context and DNA repair capacity.bioRxiv : the preprint server for biology · 2026Article
- Nucleosome spacing across cell types, diseases, and ages.Nucleic acids research · 2026Review
- FACT depletion demonstrates a role for nucleosome organization in TAD formation.Molecular systems biology · 2026Article
- Essential roles of CTCF binding sites at TAD boundaries in modulating chromatin interactions and transcriptional regulation at theFrontiers in immunology · 2025Article
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Authors and funding
9 authors.
Funding
Abstract
CTCF binding sites serve as anchors for the 3D chromatin architecture in vertebrates. The functionality of these anchors is influenced by the residence time of CTCF on chromatin, which is determined by its binding affinity and its interactions with nucleosomes and other chromatin-associated factors. In this study, we demonstrate that CTCF occupancy is driven by CTCF motifs, strategically positioned at the entry sides of a well-positioned nucleosome, such that, upon binding, the N-terminus of CTCF is oriented towards the nucleosome. We refer to this nucleosome as the CTCF priming nucleosome (CPN). Our analyses suggest that CTCF can more easily displace the CPN if the nucleosome is not marked by CpG methylation or repressive histone modifications. Under these permissive conditions, the N-terminus of CTCF recruits SMARCA5 to reposition the CPN downstream, thereby creating nucleosome-free regions that enhance CTCF occupancy and cohesin stalling. In contrast, when CPNs carry repressive epigenetic marks, CTCF binding is weaker, with no nucleosome displacement or chromatin opening, and cohesin is retained less effectively at CTCF binding sites. We propose that the epigenetic status of CPNs shapes cell-specific CTCF binding patterns, ensuring the maintenance of chromatin architecture throughout the cell cycle.
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