Evidence map›Paper›PMID 30842216›Full record

ArticleGenes & development2019

The Set1 complex is dimeric and acts with Jhd2 demethylation to convey symmetrical H3K4 trimethylation.

Rupam Choudhury, Sukhdeep Singh, Senthil Arumugam, Assen Roguev, A Francis Stewart

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
–field-weighted citation impact
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

21 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Histone sumoylation and chromatin dynamics.Nucleic acids research · 2021
    Review
  19. The complex activities of the SET1/MLL complex core subunits in development and disease.Biochimica et biophysica acta. Gene regulatory mechanisms · 2020
    Review
  20. Review
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

5 authors at 3 institutions in 3 countries.

Rupam ChoudhuryGenomics, Biotechnology Center, Center for Molecular and Cellular Bioengineering, University of Technology Dresden, 01307 Dresden, Germany.
Sukhdeep SinghGenomics, Biotechnology Center, Center for Molecular and Cellular Bioengineering, University of Technology Dresden, 01307 Dresden, Germany.
Senthil ArumugamEuropean Molecular Biology Laboratory Australia Node for Single Molecule Science, ARC Centre of Excellence in Advanced Molecular Imaging, School of Medical Sciences, University of New South Wales, Sydney 2052, Australia.
Assen RoguevGenomics, Biotechnology Center, Center for Molecular and Cellular Bioengineering, University of Technology Dresden, 01307 Dresden, Germany.ORCID 0000-0003-3470-747X
A Francis StewartGenomics, Biotechnology Center, Center for Molecular and Cellular Bioengineering, University of Technology Dresden, 01307 Dresden, Germany.ORCID 0000-0002-4754-1707
Center for Systems Biology Dresden · DEUniversity of California, San Francisco · USUNSW Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epigenetic modifications can maintain or alter the inherent symmetry of the nucleosome. However, the mechanisms that deposit and/or propagate symmetry or asymmetry are not understood. Here we report that yeast Set1C/COMPASS (complex of proteins associated with Set1) is dimeric and, consequently, symmetrically trimethylates histone 3 Lys4 (H3K4me3) on promoter nucleosomes. Mutation of the dimer interface to make Set1C monomeric abolished H3K4me3 on most promoters. The most active promoters, particularly those involved in the oxidative phase of the yeast metabolic cycle, displayed H3K4me2, which is normally excluded from active promoters, and a subset of these also displayed H3K4me3. In wild-type yeast, deletion of the sole H3K4 demethylase, Jhd2, has no effect. However, in monomeric Set1C yeast, Jhd2 deletion increased H3K4me3 levels on the H3K4me2 promoters. Notably, the association of Set1C with the elongating polymerase was not perturbed by monomerization. These results imply that symmetrical H3K4 methylation is an embedded consequence of Set1C dimerism and that Jhd2 demethylates asymmetric H3K4me3. Consequently, rather than methylation and demethylation acting in opposition as logic would suggest, a dimeric methyltransferase and monomeric demethylase cooperate to eliminate asymmetry and focus symmetrical H3K4me3 onto selected nucleosomes. This presents a new paradigm for the establishment of epigenetic detail.

Indexed as

DemethylationDimerizationEpigenesis, GeneticGene DeletionHistonesJumonji Domain-Containing Histone DemethylasesMethylationMutagenesisNucleosomesSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsTranscription, GeneticHistonesJumonji Domain-Containing Histone DemethylasesNucleosomesSaccharomyces cerevisiae Proteinschromatinepigeneticshistone demethylationhistone methylationpromoter architecture

Identifiers

PMID30842216
PMCPMC6499330
OpenAlexW2900841864

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.