Evidence map›Paper›PMID 20393567›Full record

ArticleNature2010

CpG islands influence chromatin structure via the CpG-binding protein Cfp1.

John P Thomson, Peter J Skene, Jim Selfridge, Thomas Clouaire, Jacky Guy, Shaun Webb, Alastair R W Kerr, Aimée Deaton, Rob Andrews, Keith D James and 3 more

Open access · greenAbstract read
In one paragraph

Article in Nature, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 334 papers.

0numbers the graph read from it
0cells of the map it votes in
334citing papers in PubMed
32.3field-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

334 citing papers in PubMed, 642 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

274 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 1 country.

John P ThomsonWellcome Trust Centre for Cell Biology, Michael Swann Building, University of Edinburgh, Mayfield Road, Edinburgh EH9 3JR, UK.
Peter J Skene
Jim Selfridge
Thomas Clouaire
Jacky Guy
Shaun Webb
Alastair R W Kerr
Aimée Deaton
Rob Andrews
Keith D James
Daniel J Turner
Robert Illingworth
Adrian Bird
Wellcome Centre for Cell Biology · GBUniversity of Edinburgh · GBWellcome Sanger Institute · GB

Funding

Cancer Research UKMedical Research Council G0800026Wellcome Trust 079643Wellcome Trust 091580Wellcome Trust 098051
6 · The paper itself

Abstract

CpG islands (CGIs) are prominent in the mammalian genome owing to their GC-rich base composition and high density of CpG dinucleotides. Most human gene promoters are embedded within CGIs that lack DNA methylation and coincide with sites of histone H3 lysine 4 trimethylation (H3K4me3), irrespective of transcriptional activity. In spite of these intriguing correlations, the functional significance of non-methylated CGI sequences with respect to chromatin structure and transcription is unknown. By performing a search for proteins that are common to all CGIs, here we show high enrichment for Cfp1, which selectively binds to non-methylated CpGs in vitro. Chromatin immunoprecipitation of a mono-allelically methylated CGI confirmed that Cfp1 specifically associates with non-methylated CpG sites in vivo. High throughput sequencing of Cfp1-bound chromatin identified a notable concordance with non-methylated CGIs and sites of H3K4me3 in the mouse brain. Levels of H3K4me3 at CGIs were markedly reduced in Cfp1-depleted cells, consistent with the finding that Cfp1 associates with the H3K4 methyltransferase Setd1 (refs 7, 8). To test whether non-methylated CpG-dense sequences are sufficient to establish domains of H3K4me3, we analysed artificial CpG clusters that were integrated into the mouse genome. Despite the absence of promoters, the insertions recruited Cfp1 and created new peaks of H3K4me3. The data indicate that a primary function of non-methylated CGIs is to genetically influence the local chromatin modification state by interaction with Cfp1 and perhaps other CpG-binding proteins.

Indexed as

Chromatin Assembly and DisassemblyAllelesAnimalsBrainCell LineChromatinChromatin ImmunoprecipitationCpG IslandsDNA MethylationGenomeHistone-Lysine N-MethyltransferaseHistonesMethylationMiceNIH 3T3 CellsPromoter Regions, GeneticChromatinCxxc1 protein, mouseHistone-Lysine N-MethyltransferaseHistonesTrans-Activators

Identifiers

PMID20393567
PMCPMC3730110
OpenAlexW2010291571

What OpenQuestion holds

Textmetadata
LicenceTDM
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.