Evidence map›Paper›PMID 33247104›Full record

ArticleNature communications2020

Transcription-dependent cohesin repositioning rewires chromatin loops in cellular senescence.

Ioana Olan, Aled J Parry, Stefan Schoenfelder, Masako Narita, Yoko Ito, Adelyne S L Chan, Guy St C Slater, Dóra Bihary, Masashige Bando, Katsuhiko Shirahige and 4 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
3.4field-weighted citation impact, top 6% 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

48 citing papers in PubMed, 80 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Interrogating the regulatory epigenome of cellular senescence.Cellular and molecular life sciences : CMLS · 2025
    Review
  8. Review
  9. Article
  10. Bridging spatial and temporal scales of developmental gene regulation.Current opinion in genetics & development · 2025
    Review
  11. Article
  12. Article
  13. Article
  14. Transcriptional machinery as an architect of genome structure.Current opinion in structural biology · 2024
    Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article
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

14 authors at 5 institutions in 3 countries.

Ioana OlanCancer Research UK Cambridge Institute, University of Cambridge, Robinson Way, Cambridge, UK.ORCID 0000-0003-0692-1831
Aled J ParryCancer Research UK Cambridge Institute, University of Cambridge, Robinson Way, Cambridge, UK.ORCID 0000-0001-5192-3727
Stefan SchoenfelderEpigenetics Programme, The Babraham Institute, Babraham Research Campus, Cambridge, UK.ORCID 0000-0002-3200-8133
Masako NaritaCancer Research UK Cambridge Institute, University of Cambridge, Robinson Way, Cambridge, UK.ORCID 0000-0002-9774-4908
Yoko ItoCancer Research UK Cambridge Institute, University of Cambridge, Robinson Way, Cambridge, UK.ORCID 0000-0003-4578-6126
Adelyne S L ChanCancer Research UK Cambridge Institute, University of Cambridge, Robinson Way, Cambridge, UK.
Guy St C SlaterCancer Research UK Cambridge Institute, University of Cambridge, Robinson Way, Cambridge, UK.
Dóra BiharyMRC Cancer Unit, Hutchison/MRC Research Centre, University of Cambridge, Cambridge Biomedical Campus, Cambridge, UK.ORCID 0000-0001-7871-7288
Masashige BandoLaboratory of Genome Structure and Function, Institute of Molecular and Cellular Biosciences, The University of Tokyo, Tokyo, Japan.
Katsuhiko ShirahigeLaboratory of Genome Structure and Function, Institute of Molecular and Cellular Biosciences, The University of Tokyo, Tokyo, Japan.
Hiroshi KimuraCell Biology Centre, Institute of Innovative Research, Tokyo Institute of Technology, Yokohama, Japan.ORCID 0000-0003-0854-083X
Shamith A SamarajiwaMRC Cancer Unit, Hutchison/MRC Research Centre, University of Cambridge, Cambridge Biomedical Campus, Cambridge, UK.ORCID 0000-0003-1046-0601
Peter FraserNuclear Dynamics Programme, The Babraham Institute, Babraham Research Campus, Cambridge, UK. pfraser@bio.fsu.edu.ORCID 0000-0002-0041-1227
Masashi NaritaCancer Research UK Cambridge Institute, University of Cambridge, Robinson Way, Cambridge, UK. masashi.narita@cruk.cam.ac.uk.ORCID 0000-0001-7764-577X
University of Cambridge · GBBabraham Institute · GBThe University of Tokyo · JPTokyo Institute of Technology · JPFlorida State University · US

Funding

Biotechnology and Biological Sciences Research Council BB/J004480/1Biotechnology and Biological Sciences Research Council BB/S013466/1Cancer Research UK 24453Cancer Research UK 30462Cancer Research UK C9545/A29580Medical Research Council MC_UU_12022/10Medical Research Council MR/L007150/1Medical Research Council MR/M013049/1Medical Research Council MR/R010013/1Medical Research Council MR/R015724/1Medical Research Council MR/T016787/1Wellcome TrustWellcome Trust 105367/Z/14/ZWellcome Trust 215912/Z/19/Z
6 · The paper itself

Abstract

Senescence is a state of stable proliferative arrest, generally accompanied by the senescence-associated secretory phenotype, which modulates tissue homeostasis. Enhancer-promoter interactions, facilitated by chromatin loops, play a key role in gene regulation but their relevance in senescence remains elusive. Here, we use Hi-C to show that oncogenic RAS-induced senescence in human diploid fibroblasts is accompanied by extensive enhancer-promoter rewiring, which is closely connected with dynamic cohesin binding to the genome. We find de novo cohesin peaks often at the 3' end of a subset of active genes. RAS-induced de novo cohesin peaks are transcription-dependent and enriched for senescence-associated genes, exemplified by IL1B, where de novo cohesin binding is involved in new loop formation. Similar IL1B induction with de novo cohesin appearance and new loop formation are observed in terminally differentiated macrophages, but not TNFα-treated cells. These results suggest that RAS-induced senescence represents a cell fate determination-like process characterised by a unique gene expression profile and 3D genome folding signature, mediated in part through cohesin redistribution on chromatin.

Indexed as

Transcription, GeneticCCCTC-Binding FactorCell Cycle ProteinsCell DifferentiationCell LineCellular SenescenceChromatinChromosomal Proteins, Non-HistoneCohesinsEnhancer Elements, GeneticGene Expression RegulationGenetic LociGenomeHumansInterleukin-1MacrophagesCCCTC-Binding FactorCell Cycle ProteinsChromatinChromosomal Proteins, Non-HistoneCohesinsInterleukin-1ras ProteinsTumor Necrosis Factor-alpha

Identifiers

PMID33247104
PMCPMC7695716
OpenAlexW3108031567

What OpenQuestion holds

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LicenceCC BY
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.