Evidence map›Paper›PMID 25838386›Full record

ArticleScience (New York, N.Y.)2015

Epigenetics. Restricted epigenetic inheritance of H3K9 methylation.

Pauline N C B Audergon, Sandra Catania, Alexander Kagansky, Pin Tong, Manu Shukla, Alison L Pidoux, Robin C Allshire

Abstract read
In one paragraph

Article in Science (New York, N.Y.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 168 papers.

0numbers the graph read from it
0cells of the map it votes in
168citing 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

168 citing papers in PubMed.

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  6. In thePNAS nexus · 2026
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108 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

7 authors.

Pauline N C B AudergonWellcome Trust Centre for Cell Biology and Institute of Cell Biology, School of Biological Sciences, The University of Edinburgh, Max Born Crescent, Edinburgh EH9 3BF, Scotland, UK.
Sandra CataniaWellcome Trust Centre for Cell Biology and Institute of Cell Biology, School of Biological Sciences, The University of Edinburgh, Max Born Crescent, Edinburgh EH9 3BF, Scotland, UK.
Alexander KaganskyWellcome Trust Centre for Cell Biology and Institute of Cell Biology, School of Biological Sciences, The University of Edinburgh, Max Born Crescent, Edinburgh EH9 3BF, Scotland, UK.
Pin TongWellcome Trust Centre for Cell Biology and Institute of Cell Biology, School of Biological Sciences, The University of Edinburgh, Max Born Crescent, Edinburgh EH9 3BF, Scotland, UK.
Manu ShuklaWellcome Trust Centre for Cell Biology and Institute of Cell Biology, School of Biological Sciences, The University of Edinburgh, Max Born Crescent, Edinburgh EH9 3BF, Scotland, UK.
Alison L PidouxWellcome Trust Centre for Cell Biology and Institute of Cell Biology, School of Biological Sciences, The University of Edinburgh, Max Born Crescent, Edinburgh EH9 3BF, Scotland, UK.
Robin C AllshireWellcome Trust Centre for Cell Biology and Institute of Cell Biology, School of Biological Sciences, The University of Edinburgh, Max Born Crescent, Edinburgh EH9 3BF, Scotland, UK. robin.allshire@ed.ac.uk.

Funding

Wellcome Trust 092076Wellcome Trust 093852Wellcome Trust 095021
6 · The paper itself

Abstract

Posttranslational histone modifications are believed to allow the epigenetic transmission of distinct chromatin states, independently of associated DNA sequences. Histone H3 lysine 9 (H3K9) methylation is essential for heterochromatin formation; however, a demonstration of its epigenetic heritability is lacking. Fission yeast has a single H3K9 methyltransferase, Clr4, that directs all H3K9 methylation and heterochromatin. Using releasable tethered Clr4 reveals that an active process rapidly erases H3K9 methylation from tethering sites in wild-type cells. However, inactivation of the putative histone demethylase Epe1 allows H3K9 methylation and silent chromatin maintenance at the tethering site through many mitotic divisions, and transgenerationally through meiosis, after release of tethered Clr4. Thus, H3K9 methylation is a heritable epigenetic mark whose transmission is usually countered by its active removal, which prevents the unauthorized inheritance of heterochromatin.

Indexed as

Epigenesis, GeneticCell Cycle ProteinsHeterochromatinHistone-Lysine N-MethyltransferaseHistonesLysineMethylationMethyltransferasesMutationNuclear ProteinsProtein Processing, Post-TranslationalSchizosaccharomycesSchizosaccharomyces pombe ProteinsCell Cycle Proteinsclr4 protein, S pombeepe1 protein, S pombeHeterochromatinHistone-Lysine N-MethyltransferaseHistonesLysineMethyltransferasesNuclear ProteinsSchizosaccharomyces pombe Proteins

Identifiers

PMID25838386
PMCPMC4397586

What OpenQuestion holds

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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.