Journal
CELL REPORTS
Volume 32, Issue 3, Pages -Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2020.107929
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Funding
- UK Research and Innovation Medical Research Council (UKRI MRC)
- Boehringer Ingelheim
- Austrian Research Promotion Agency [FFG852936]
- European Research Council (ERC) under the European Union's Horizon 2020 research and innovation programme [693949]
- Human Frontier Science Program [RGP0057/2018]
- Vienna Science and Technology Fund [LS19-029]
- UKRI Biotechnology and Biological Science Research Council (BBSRC) [BB/J004480/1]
- MRC [MR/T016787/1]
- Babraham Institute
- BBSRC [BBS/E/B/000C0404, BBS/E/B/000C0405, BBS/E/B/000C0421] Funding Source: UKRI
- MRC [MR/T016787/1, MC_UP_1605/3, MR/R015724/1] Funding Source: UKRI
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It is currently assumed that 3D chromosomal organization plays a central role in transcriptional control. However, depletion of cohesin and CTCF affects the steady-state levels of only a minority of transcripts. Here, we use high-resolution Capture Hi-C to interrogate the dynamics of chromosomal contacts of all annotated human gene promoters upon degradation of cohesin and CTCF. We show that a majority of promoter-anchored contacts are lost in these conditions, but many contacts with distinct properties are maintained, and some new ones are gained. The rewiring of contacts between promoters and active enhancers upon cohesin degradation associates with rapid changes in target gene transcription as detected by SLAM sequencing (SLAM-seq). These results provide a mechanistic explanation for the limited, but consistent, effects of cohesin and CTCF depletion on steady-state transcription and suggest the existence of both cohesin-dependent and -in-dependent mechanisms of enhancer-promoter pairing.
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