Evidence map›Paper›PMID 31468675›Full record

ArticleEMBO reports2019

H3K14 ubiquitylation promotes H3K9 methylation for heterochromatin assembly.

Eriko Oya, Reiko Nakagawa, Yuriko Yoshimura, Mayo Tanaka, Gohei Nishibuchi, Shinichi Machida, Atsuko Shirai, Karl Ekwall, Hitoshi Kurumizaka, Hideaki Tagami and 1 more

Abstract read
In one paragraph

Article in EMBO reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing 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

43 citing papers in PubMed.

  1. Review
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  15. Clr4Nature communications · 2024
    Article
  16. Review
  17. Article
  18. Minimal requirements for the epigenetic inheritance of engineered silent chromatin domains.Proceedings of the National Academy of Sciences of the United States of America · 2024
    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

11 authors.

Eriko OyaGraduate School of Natural Sciences, Nagoya City University, Nagoya, Japan.
Reiko NakagawaLaboratory for Phyloinformatics, RIKEN Center for Biosystems Dynamics Research, Kobe, Japan.ORCID 0000-0002-6178-2945
Yuriko YoshimuraDivision of Chromatin Regulation, National Institute for Basic Biology, Okazaki, Japan.
Mayo TanakaDivision of Chromatin Regulation, National Institute for Basic Biology, Okazaki, Japan.
Gohei NishibuchiGraduate School of Natural Sciences, Nagoya City University, Nagoya, Japan.
Shinichi MachidaLaboratory of Structural Biology, Graduate School of Advanced Science and Engineering, Waseda University, Shinjuku-ku, Tokyo, Japan.
Atsuko ShiraiCellular Memory Laboratory, RIKEN, Wako, Japan.
Karl EkwallDepartment of Biosciences and Nutrition, Karolinska Institutet, Huddinge, Sweden.ORCID 0000-0002-3029-4041
Hitoshi KurumizakaLaboratory of Structural Biology, Graduate School of Advanced Science and Engineering, Waseda University, Shinjuku-ku, Tokyo, Japan.ORCID 0000-0001-7412-3722
Hideaki TagamiGraduate School of Natural Sciences, Nagoya City University, Nagoya, Japan.
Jun-Ichi NakayamaGraduate School of Natural Sciences, Nagoya City University, Nagoya, Japan.ORCID 0000-0002-5597-8239

Funding

MEXT|Japan Society for the Promotion of Science (JSPS) JP17H03713MEXT|Japan Society for the Promotion of Science (JSPS) JP18H05532MEXT|Japan Society for the Promotion of Science (JSPS) JP18H05534MEXT|Japan Society for the Promotion of Science (JSPS) JP23114005MEXT|Japan Society for the Promotion of Science (JSPS) JP26291072Mochida Memorial Foundation for Medical and Pharmaceutical ResearchSvenska Forskningsrådet Formas (Swedish Research Council Formas)Swedish Cancer SocietyTakeda Science FoundationUehara Memorial Foundation
6 · The paper itself

Abstract

The methylation of histone H3 at lysine 9 (H3K9me), performed by the methyltransferase Clr4/SUV39H, is a key event in heterochromatin assembly. In fission yeast, Clr4, together with the ubiquitin E3 ligase Cul4, forms the Clr4 methyltransferase complex (CLRC), whose physiological targets and biological role are currently unclear. Here, we show that CLRC-dependent H3 ubiquitylation regulates Clr4's methyltransferase activity. Affinity-purified CLRC ubiquitylates histone H3, and mass spectrometric and mutation analyses reveal that H3 lysine 14 (H3K14) is the preferred target of the complex. Chromatin immunoprecipitation analysis shows that H3K14 ubiquitylation (H3K14ub) is closely associated with H3K9me-enriched chromatin. Notably, the CLRC-mediated H3 ubiquitylation promotes H3K9me by Clr4, suggesting that H3 ubiquitylation is intimately linked to the establishment and/or maintenance of H3K9me. These findings demonstrate a cross-talk mechanism between histone ubiquitylation and methylation that is involved in heterochromatin assembly.

Indexed as

UbiquitinationAmino Acid SequenceHeterochromatinHistonesLysineMethylationMethyltransferasesMutationSchizosaccharomycesSchizosaccharomyces pombe ProteinsHeterochromatinHistonesLysineMethyltransferasesSchizosaccharomyces pombe Proteinsepigenetic gene silencingfission yeastheterochromatinhistone methylationhistone ubiquitylation

Identifiers

PMID31468675
PMCPMC6776926

What OpenQuestion holds

Textmetadata
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.