ArticleNature communications2024
Cell-type differential targeting of SETDB1 prevents aberrant CTCF binding, chromatin looping, and cis-regulatory interactions.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 44 citations in OpenAlex.
- Review
- Targeting SUV39H2 exon skipping reverses resistance to CDK4/6 inhibitors via transcriptional activation of p21.Science advances · 2026Article
- WAVE2 and REST/NRSF Regulate Clustered Gene Expression by Maintaining Heterochromatin Organization.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Article
- IAPEz retrotransposons regulate the first lineage segregation in mouse pre-implantation development.Nucleic acids research · 2026Article
- H3K9me3 controls epidermis morphogenesis by regulating RNA Pol II dynamics at developmental promoters and enhancers.Nature communications · 2026Article
- The Many Faces of SetDB1.Epigenomes · 2026Review
- HiCMamba: Enhancing Hi-C resolution and identifying 3D genome structures with state space modeling.PLoS computational biology · 2026Article
- Missense substitutions in the BTB domain of ZBTB24 can lead to protein instability and cause ICF2 syndrome.Human molecular genetics · 2026Article
- 3D enhancer architecture coordinated by CTCF determines immune-related gene expression patterns via RNA polymerase II pause-release in CD4+ T cells.Nucleic acids research · 2025Article
- PB-DiffHiC: a statistical framework for detecting differential chromatin interactions from high resolution pseudo-bulk Hi-C data.BMC genomics · 2025Article
- H3K27 and H3K9 methylation mask potential CTCF binding sites to maintain 3D genome integrity.Genome research · 2025Article
- CTCF binding landscape is shaped by the epigenetic state of the N-terminal nucleosome in relation to CTCF motif orientation.Nucleic acids research · 2025Article
- Deciphering the role of histone modifications in memory and exhausted CD8 T cells.Scientific reports · 2025Article
- Incorporating multiscale methylation effects into nucleosome-resolution chromatin models for simulating mesoscale fibers.The Journal of chemical physics · 2025Article
- The chromatin tapestry as a framework for neurodevelopment.Genome research · 2024Review
- RNAi Knockdown ofGenes · 2024Article
- SETDB1 regulates short interspersed nuclear elements and chromatin loop organization in mouse neural precursor cells.Genome biology · 2024Article
- SETDB1 deletion causes DNA demethylation and upregulation of multiple zinc-finger genes.Molecular biology reports · 2024Article
- Mechanistic drivers of chromatin organization into compartments.Current opinion in genetics & development · 2024Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
SETDB1 is an essential histone methyltransferase that deposits histone H3 lysine 9 trimethylation (H3K9me3) to transcriptionally repress genes and repetitive elements. The function of differential H3K9me3 enrichment between cell-types remains unclear. Here, we demonstrate mutual exclusivity of H3K9me3 and CTCF across mouse tissues from different developmental timepoints. We analyze SETDB1 depleted cells and discover that H3K9me3 prevents aberrant CTCF binding independently of DNA methylation and H3K9me2. Such sites are enriched with SINE B2 retrotransposons. Moreover, analysis of higher-order genome architecture reveals that large chromatin structures including topologically associated domains and subnuclear compartments, remain intact in SETDB1 depleted cells. However, chromatin loops and local 3D interactions are disrupted, leading to transcriptional changes by modifying pre-existing chromatin landscapes. Specific genes with altered expression show differential interactions with dysregulated cis-regulatory elements. Collectively, we find that cell-type specific targets of SETDB1 maintain cellular identities by modulating CTCF binding, which shape nuclear architecture and transcriptomic networks.
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