ArticleScientific reports2025
Active regulatory elements recruit cohesin to establish cell specific chromatin domains.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Zone equalisation normalisation for improved alignment of epigenetic signal.Bioinformatics (Oxford, England) · 2026Article
- Article
- Facilitators may represent a new class of regulatory elements.Current opinion in genetics & development · 2026Review
- A functional overlap between actively transcribed genes and chromatin insulator elements.The EMBO journal · 2026Article
- The role of cohesin loading at enhancers in the flux of loop extrusion and long-range transcriptional control.bioRxiv : the preprint server for biology · 2026Article
- Stress-induced loss of CTCF reveals an alternative, promoter-based mode of cohesin looping.bioRxiv : the preprint server for biology · 2025Article
- Epigenetic Regulation of Erythropoiesis: From Developmental Programs to Therapeutic Targets.International journal of molecular sciences · 2025Review
- scATAC-seq generates more accurate and complete regulatory maps than bulk ATAC-seq.Scientific reports · 2025Article
- The α-globin super-enhancer acts in an orientation-dependent manner.Nature communications · 2025Article
- Transcriptional machinery as an architect of genome structure.Current opinion in structural biology · 2024Review
- The Wild West of spike-in normalization.Nature biotechnology · 2024Article
- Potential roles of inter-chromosomal interactions in cell fate determination.Frontiers in cell and developmental biology · 2024Review
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
As the 3D structure of the genome is analysed at ever increasing resolution it is clear that there is considerable variation in the 3D chromatin architecture across different cell types. It has been proposed that this may, in part, be due to increased recruitment of cohesin to activated cis-elements (enhancers and promoters) leading to cell-type specific loop extrusion underlying the formation of new sub-TADs. Here we show that cohesin correlates well with the presence of active enhancers and that this varies in an allele-specific manner with the presence or absence of polymorphic enhancers which vary from one individual to another. Using the alpha globin cluster as a model, we show that when all enhancers are removed, peaks of cohesin disappear from these regions and the erythroid specific sub-TAD is no longer formed. Re-insertion of the major alpha globin enhancer (R2) is associated with re-establishment of recruitment and increased interactions. In complementary experiments insertion of the R2 enhancer element into a "neutral" region of the genome recruits cohesin, induces transcription and creates a new large (75 kb) erythroid-specific domain. Together these findings support the proposal that active enhancers recruit cohesin, stimulate loop extrusion and promote the formation of cell specific sub-TADs.
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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.