Evidence map›Paper›PMID 32698000›Full record

ArticleCell reports2020

Cohesin-Dependent and -Independent Mechanisms Mediate Chromosomal Contacts between Promoters and Enhancers.

Michiel J Thiecke, Gordana Wutz, Matthias Muhar, Wen Tang, Stephen Bevan, Valeriya Malysheva, Roman Stocsits, Tobias Neumann, Johannes Zuber, Peter Fraser and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.

0numbers the graph read from it
0cells of the map it votes in
107citing papers in PubMed
9.9field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

107 citing papers in PubMed, 177 citations in OpenAlex.

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  18. Single-Molecule Analyses of Human Cohesin Complex.Methods in molecular biology (Clifton, N.J.) · 2026
    Article
  19. Article
  20. Article

47 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 3 institutions in 3 countries.

Michiel J ThieckeNuclear Dynamics Programme, Babraham Institute, Cambridge CB22 3AT, UK.
Gordana WutzResearch Institute of Molecular Pathology, Vienna Biocenter, Vienna 1030, Austria.
Matthias MuharResearch Institute of Molecular Pathology, Vienna Biocenter, Vienna 1030, Austria.
Wen TangResearch Institute of Molecular Pathology, Vienna Biocenter, Vienna 1030, Austria.
Stephen BevanNuclear Dynamics Programme, Babraham Institute, Cambridge CB22 3AT, UK; Epigenetics Programme, Babraham Institute, Cambridge CB22 3AT, UK.
Valeriya MalyshevaNuclear Dynamics Programme, Babraham Institute, Cambridge CB22 3AT, UK; MRC London Institute of Medical Sciences, London W12 0NN, UK; Institute of Clinical Sciences, Faculty of Medicine, Imperial College, London W12 0NN, UK.
Roman StocsitsResearch Institute of Molecular Pathology, Vienna Biocenter, Vienna 1030, Austria.
Tobias NeumannResearch Institute of Molecular Pathology, Vienna Biocenter, Vienna 1030, Austria.
Johannes ZuberResearch Institute of Molecular Pathology, Vienna Biocenter, Vienna 1030, Austria.
Peter FraserNuclear Dynamics Programme, Babraham Institute, Cambridge CB22 3AT, UK; Department of Biological Science, Florida State University, Tallahassee, FL 32301, USA.
Stefan SchoenfelderNuclear Dynamics Programme, Babraham Institute, Cambridge CB22 3AT, UK; Epigenetics Programme, Babraham Institute, Cambridge CB22 3AT, UK.
Jan-Michael PetersResearch Institute of Molecular Pathology, Vienna Biocenter, Vienna 1030, Austria.
Mikhail SpivakovNuclear Dynamics Programme, Babraham Institute, Cambridge CB22 3AT, UK; MRC London Institute of Medical Sciences, London W12 0NN, UK; Institute of Clinical Sciences, Faculty of Medicine, Imperial College, London W12 0NN, UK. Electronic address: mikhail.spivakov@lms.mrc.ac.uk.
Research Institute of Molecular Pathology · ATBabraham Institute · GBFlorida State University · US

Funding

Biotechnology and Biological Sciences Research Council BB/J004480/1Medical Research Council MC_UP_1605/3Medical Research Council MR/R015724/1Medical Research Council MR/T016787/1
6 · The paper itself

Abstract

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 -independent mechanisms of enhancer-promoter pairing.

Indexed as

Promoter Regions, GeneticCell Cycle ProteinsChromatinChromosomal Proteins, Non-HistoneChromosomesCohesinsDNA-Binding ProteinsEnhancer Elements, GeneticGene Expression RegulationHeLa CellsHumansTranscription, GeneticCell Cycle ProteinsChromatinChromosomal Proteins, Non-HistoneCohesinsDNA-Binding ProteinscohesinCTCFpromoter capture Hi-Cpromoter-enhancer interactionsSLAM-seqtranscriptional regulation

Identifiers

PMID32698000
PMCPMC7383238
OpenAlexW3044693806

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.