ArticleGenome research2014
Nucleosome repositioning links DNA (de)methylation and differential CTCF binding during stem cell development.
Article in Genome research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.
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Who cites it
87 citing papers in PubMed, 160 citations in OpenAlex.
- Paternal Combined Botanicals Contribute to the Prevention of Estrogen Receptor-Negative Mammary Cancer in Transgenic Mice.The Journal of nutrition · 2023Trial
- Nucleosome spacing across cell types, diseases, and ages.Nucleic acids research · 2026Review
- Super-enhancer DNA methylation in cancer: the mechanism of action and therapeutic directions.Frontiers in oncology · 2025Review
- Article
- Single-stranded pre-methylated 5mC adapters uncover the methylation profile of plasma ultrashort Single-stranded cell-free DNA.Nucleic acids research · 2024Article
- Nucleosome reorganisation in breast cancer tissues.Clinical epigenetics · 2024Article
- The impact of DNA methylation on CTCF-mediated 3D genome organization.Nature structural & molecular biology · 2024Review
- Detection of new pioneer transcription factors as cell-type-specific nucleosome binders.eLife · 2024Article
- Nucleosome repositioning in chronic lymphocytic leukemia.Genome research · 2023Article
- Identification of mammalian transcription factors that bind to inaccessible chromatin.Nucleic acids research · 2023Article
- DNA strand asymmetry generated by CpG hemimethylation has opposing effects on CTCF binding.Nucleic acids research · 2023Article
- Histone exchange sensors reveal variant specific dynamics in mouse embryonic stem cells.Nature communications · 2023Article
- Review
- Epigenetic signals that direct cell type-specific interferon beta response in mouse cells.Life science alliance · 2023Article
- Diverse silent chromatin states modulate genome compartmentalization and loop extrusion barriers.Nature structural & molecular biology · 2023Article
- Enhanced nucleosome assembly at CpG sites containing an extended 5-methylcytosine analogue.Nucleic acids research · 2022Article
- Mechanisms that regulate the activities of TET proteins.Cellular and molecular life sciences : CMLS · 2022Review
- NucPosDB: a database of nucleosome positioning in vivo and nucleosomics of cell-free DNA.Chromosoma · 2022Article
- DNA sequence-dependent formation of heterochromatin nanodomains.Nature communications · 2022Article
- DNA methylation cues in nucleosome geometry, stability and unwrapping.Nucleic acids research · 2022Article
27 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During differentiation of embryonic stem cells, chromatin reorganizes to establish cell type-specific expression programs. Here, we have dissected the linkages between DNA methylation (5mC), hydroxymethylation (5hmC), nucleosome repositioning, and binding of the transcription factor CTCF during this process. By integrating MNase-seq and ChIP-seq experiments in mouse embryonic stem cells (ESC) and their differentiated counterparts with biophysical modeling, we found that the interplay between these factors depends on their genomic context. The mostly unmethylated CpG islands have reduced nucleosome occupancy and are enriched in cell type-independent binding sites for CTCF. The few remaining methylated CpG dinucleotides are preferentially associated with nucleosomes. In contrast, outside of CpG islands most CpGs are methylated, and the average methylation density oscillates so that it is highest in the linker region between nucleosomes. Outside CpG islands, binding of TET1, an enzyme that converts 5mC to 5hmC, is associated with labile, MNase-sensitive nucleosomes. Such nucleosomes are poised for eviction in ESCs and become stably bound in differentiated cells where the TET1 and 5hmC levels go down. This process regulates a class of CTCF binding sites outside CpG islands that are occupied by CTCF in ESCs but lose the protein during differentiation. We rationalize this cell type-dependent targeting of CTCF with a quantitative biophysical model of competitive binding with the histone octamer, depending on the TET1, 5hmC, and 5mC state.
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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.