Evidence map›Paper›PMID 21811414›Full record

ArticlePLoS genetics2011

Histone crosstalk directed by H2B ubiquitination is required for chromatin boundary integrity.

Meiji Kit-Wan Ma, Carol Heath, Alan Hair, Adam G West

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

23 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. RPA-mediated recruitment of Bre1 couples histone H2B ubiquitination to DNA replication and repair.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Histone modifications as regulators of life and death inMicrobial cell (Graz, Austria) · 2015
    Review
  12. Identification of a functional hotspot on ubiquitin required for stimulation of methyltransferase activity on chromatin.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  13. Review
  14. Article
  15. Epigenetic mechanisms of memory formation and reconsolidation.Neurobiology of learning and memory · 2014
    Review
  16. Epigenetic dysregulation by nickel through repressive chromatin domain disruption.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  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

4 authors at 1 institution in 1 country.

Meiji Kit-Wan MaInstitute of Cancer Sciences, College of Medical, Veterinary, and Life Sciences, University of Glasgow, Glasgow, United Kingdom.
Carol Heath
Alan Hair
Adam G West
University of Glasgow · GB

Funding

Biotechnology and Biological Sciences Research Council BBS/B/08043Medical Research Council G0400180
6 · The paper itself

Abstract

Genomic maps of chromatin modifications have provided evidence for the partitioning of genomes into domains of distinct chromatin states, which assist coordinated gene regulation. The maintenance of chromatin domain integrity can require the setting of boundaries. The HS4 insulator element marks the 3' boundary of a heterochromatin region located upstream of the chicken β-globin gene cluster. Here we show that HS4 recruits the E3 ligase RNF20/BRE1A to mediate H2B mono-ubiquitination (H2Bub1) at this insulator. Knockdown experiments show that RNF20 is required for H2Bub1 and processive H3K4 methylation. Depletion of RNF20 results in a collapse of the active histone modification signature at the HS4 chromatin boundary, where H2Bub1, H3K4 methylation, and hyperacetylation of H3, H4, and H2A.Z are rapidly lost. A remarkably similar set of events occurs at the HSA/HSB regulatory elements of the FOLR1 gene, which mark the 5' boundary of the same heterochromatin region. We find that persistent H2Bub1 at the HSA/HSB and HS4 elements is required for chromatin boundary integrity. The loss of boundary function leads to the sequential spreading of H3K9me2, H3K9me3, and H4K20me3 over the entire 50 kb FOLR1 and β-globin region and silencing of FOLR1 expression. These findings show that the HSA/HSB and HS4 boundary elements direct a cascade of active histone modifications that defend the FOLR1 and β-globin gene loci from the pervasive encroachment of an adjacent heterochromatin domain. We propose that many gene loci employ H2Bub1-dependent boundaries to prevent heterochromatin spreading.

Indexed as

UbiquitinationAcetylationAmino Acid SequenceAnimalsAvian Proteinsbeta-GlobinsBlotting, WesternCell Line, TumorChick EmbryoChickensChromatinFolate Receptor 1HeterochromatinHistone CodeHistonesInsulator ElementsAvian Proteinsbeta-GlobinsChromatinFolate Receptor 1HeterochromatinHistonesLysineRNA Polymerase IIUbiquitin-Protein Ligases

Identifiers

PMID21811414
PMCPMC3140996
OpenAlexW2017006362

What OpenQuestion holds

Textmetadata
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.