Evidence map›Paper›PMID 27705745›Full record

ArticleeLife2016

RYBP stimulates PRC1 to shape chromatin-based communication between Polycomb repressive complexes.

Nathan R Rose, Hamish W King, Neil P Blackledge, Nadezda A Fursova, Katherine Ji Ember, Roman Fischer, Benedikt M Kessler, Robert J Klose

Open access · goldAbstract read
In one paragraph

Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

91 citing papers in PubMed, 151 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. De novo variants in RYBP are associated with a severe neurodevelopmental disorder and congenital anomalies.Genetics in medicine : official journal of the American College of Medical Genetics · 2025
    Article
  16. Review
  17. Article
  18. Polycomb protein RYBP facilitates super-enhancer activity.Molecular medicine (Cambridge, Mass.) · 2024
    Article
  19. Article
  20. Article

31 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

8 authors at 1 institution in 1 country.

Nathan R RoseDepartment of Biochemistry, University of Oxford, Oxford, United Kingdom.
Hamish W KingDepartment of Biochemistry, University of Oxford, Oxford, United Kingdom.
Neil P BlackledgeDepartment of Biochemistry, University of Oxford, Oxford, United Kingdom.
Nadezda A FursovaDepartment of Biochemistry, University of Oxford, Oxford, United Kingdom.
Katherine Ji EmberDepartment of Biochemistry, University of Oxford, Oxford, United Kingdom.
Roman FischerTDI Mass Spectrometry Laboratory, Target Discovery Institute, University of Oxford, Oxford, United Kingdom.ORCID 0000-0002-9715-5951
Benedikt M KesslerTDI Mass Spectrometry Laboratory, Target Discovery Institute, University of Oxford, Oxford, United Kingdom.
Robert J KloseDepartment of Biochemistry, University of Oxford, Oxford, United Kingdom.ORCID 0000-0002-8726-7888
University of Oxford · GB

Funding

Wellcome TrustWellcome Trust 097813/Z/11/ZWellcome Trust 098024/Z/11/Z
6 · The paper itself

Abstract

Polycomb group (PcG) proteins function as chromatin-based transcriptional repressors that are essential for normal gene regulation during development. However, how these systems function to achieve transcriptional regulation remains very poorly understood. Here, we discover that the histone H2AK119 E3 ubiquitin ligase activity of Polycomb repressive complex 1 (PRC1) is defined by the composition of its catalytic subunits and is highly regulated by RYBP/YAF2-dependent stimulation. In mouse embryonic stem cells, RYBP plays a central role in shaping H2AK119 mono-ubiquitylation at PcG targets and underpins an activity-based communication between PRC1 and Polycomb repressive complex 2 (PRC2) which is required for normal histone H3 lysine 27 trimethylation (H3K27me3). Without normal histone modification-dependent communication between PRC1 and PRC2, repressive Polycomb chromatin domains can erode, rendering target genes susceptible to inappropriate gene expression signals. This suggests that activity-based communication and histone modification-dependent thresholds create a localized form of epigenetic memory required for normal PcG chromatin domain function in gene regulation.

Indexed as

Epigenetic RepressionTranscription, GeneticAnimalsChromatinHistonesMethylationMiceMouse Embryonic Stem CellsMuscle ProteinsPolycomb-Group ProteinsPolycomb Repressive Complex 1Protein Processing, Post-TranslationalRepressor ProteinsChromatinHistonesMuscle ProteinsPolycomb-Group ProteinsPolycomb Repressive Complex 1Repressor ProteinsRybp protein, mouseYaf2 protein, mousechromatinchromosomesE3 ubiquitin ligasegene expressiongeneshistone modificationmousePolycomb repressive complex

Identifiers

PMID27705745
PMCPMC5065315
OpenAlexW2529278390

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.