Evidence map›Paper›PMID 23451023›Full record

ArticlePloS one2013

H3K56me3 is a novel, conserved heterochromatic mark that largely but not completely overlaps with H3K9me3 in both regulation and localization.

Antonia P M Jack, Silva Bussemer, Matthias Hahn, Sebastian Pünzeler, Martha Snyder, Michael Wells, Gyorgyi Csankovszki, Irina Solovei, Gunnar Schotta, Sandra B Hake

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

39 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
  2. The GNMT N-terminus Couples Folate Feedback to Methyl-donor Homeostasis.bioRxiv : the preprint server for biology · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. KDM4 Demethylases: Structure, Function, and Inhibitors.Advances in experimental medicine and biology · 2023
    Article
  8. Review
  9. Article
  10. Targets of histone H3 lysine 9 methyltransferases.Frontiers in cell and developmental biology · 2022
    Review
  11. Article
  12. Article
  13. Mechanistic insights into KDM4A driven genomic instability.Biochemical Society transactions · 2021
    Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Review
  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

10 authors at 4 institutions in 2 countries.

Antonia P M JackCenter for Integrated Protein Science Munich, Adolf-Butenandt-Institute, Department of Molecular Biology, Ludwig-Maximilians-University Munich, Munich, Germany.
Silva Bussemer
Matthias Hahn
Sebastian Pünzeler
Martha Snyder
Michael Wells
Gyorgyi Csankovszki
Irina Solovei
Gunnar Schotta
Sandra B Hake
Ludwig-Maximilians-Universität München · DECenter for Integrated Protein Science Munich · DEUniversity of Michigan–Ann Arbor · USMichigan United · US

Funding

The Dosage Compensation Machinery of C. ElegansR01GM079533 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CSANKOVSZKI, GYORGYI · 2007 to 2015
$2.5M
NIGMS NIH HHS R01 GM079533
6 · The paper itself

Abstract

Histone lysine (K) methylation has been shown to play a fundamental role in modulating chromatin architecture and regulation of gene expression. Here we report on the identification of histone H3K56, located at the pivotal, nucleosome DNA entry/exit point, as a novel methylation site that is evolutionary conserved. We identify trimethylation of H3K56 (H3K56me3) as a modification that is present during all cell cycle phases, with the exception of S-phase, where it is underrepresented on chromatin. H3K56me3 is a novel heterochromatin mark, since it is enriched at pericentromeres but not telomeres and is thereby similar, but not identical, to the localization of H3K9me3 and H4K20me3. Possibly due to H3 sequence similarities, Suv39h enzymes, responsible for trimethylation of H3K9, also affect methylation of H3K56. Similarly, we demonstrate that trimethylation of H3K56 is removed by members of the JMJD2 family of demethylases that also target H3K9me3. Furthermore, we identify and characterize mouse mJmjd2E and its human homolog hKDM4L as novel, functionally active enzymes that catalyze the removal of two methyl groups from trimethylated H3K9 and K56. H3K56me3 is also found in C. elegans, where it co-localizes with H3K9me3 in most, but not all, tissues. Taken together, our findings raise interesting questions regarding how methylation of H3K9 and H3K56 is regulated in different organisms and their functional roles in heterochromatin formation and/or maintenance.

Indexed as

AnimalsCell CycleCell LineChromatinDNA MethylationHeLa CellsHeterochromatinHistonesHumansLysineMethylationMiceMicroscopy, FluorescencePolymerase Chain ReactionChromatinHeterochromatinHistonesLysine

Identifiers

PMID23451023
PMCPMC3579866
OpenAlexW2079304435

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.