Evidence map›Paper›PMID 24244179›Full record

ArticlePLoS genetics2013

Ash1l methylates Lys36 of histone H3 independently of transcriptional elongation to counteract polycomb silencing.

Hitomi Miyazaki, Ken Higashimoto, Yukari Yada, Takaho A Endo, Jafar Sharif, Toshiharu Komori, Masashi Matsuda, Yoko Koseki, Manabu Nakayama, Hidenobu Soejima and 4 more

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% 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

60 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.

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  8. Loss-of-function mutations of microRNA-142-3p promoteWorld journal of gastroenterology · 2025
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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

14 authors at 6 institutions in 1 country.

Hitomi MiyazakiDivision of Molecular Genetics and Epigenetics, Department of Biomolecular Sciences, Faculty of Medicine, Saga University, 5-1-1 Nabeshima, Saga City, Saga, Japan ; Precursory Research for Embryonic Science and Technology (PRESTO), Japan Science and Technology Agency (JST), 4-1-8 Honcho, Kawaguchi City, Saitama, Japan.
Ken Higashimoto
Yukari Yada
Takaho A Endo
Jafar Sharif
Toshiharu Komori
Masashi Matsuda
Yoko Koseki
Manabu Nakayama
Hidenobu Soejima
Hiroshi Handa
Haruhiko Koseki
Susumu Hirose
Kenichi Nishioka
RIKEN Center for Integrative Medical Sciences · JPNational Institute of Genetics · JPSaga University · JPJapan Science and Technology Agency · JPKazusa DNA Research Institute · JPTokyo Institute of Technology · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Molecular mechanisms for the establishment of transcriptional memory are poorly understood. 5,6-dichloro-1-D-ribofuranosyl-benzimidazole (DRB) is a P-TEFb kinase inhibitor that artificially induces the poised RNA polymerase II (RNAPII), thereby manifesting intermediate steps for the establishment of transcriptional activation. Here, using genetics and DRB, we show that mammalian Absent, small, or homeotic discs 1-like (Ash1l), a member of the trithorax group proteins, methylates Lys36 of histone H3 to promote the establishment of Hox gene expression by counteracting Polycomb silencing. Importantly, we found that Ash1l-dependent Lys36 di-, tri-methylation of histone H3 in a coding region and exclusion of Polycomb group proteins occur independently of transcriptional elongation in embryonic stem (ES) cells, although both were previously thought to be consequences of transcription. Genome-wide analyses of histone H3 Lys36 methylation under DRB treatment have suggested that binding of the retinoic acid receptor (RAR) to a certain genomic region promotes trimethylation in the RAR-associated gene independent of its ongoing transcription. Moreover, DRB treatment unveils a parallel response between Lys36 methylation of histone H3 and occupancy of either Tip60 or Mof in a region-dependent manner. We also found that Brg1 is another key player involved in the response. Our results uncover a novel regulatory cascade orchestrated by Ash1l with RAR and provide insights into mechanisms underlying the establishment of the transcriptional activation that counteracts Polycomb silencing.

Indexed as

Transcription, GeneticAnimalsChromatinDichlororibofuranosylbenzimidazoleDNA-Binding ProteinsDrosophila melanogasterDrosophila ProteinsGene SilencingHistone AcetyltransferasesHistone-Lysine N-MethyltransferaseHistonesHumansLysineMethylationNuclear ProteinsPolycomb-Group ProteinsASH1L protein, humanChromatinDichlororibofuranosylbenzimidazoleDNA-Binding ProteinsDrosophila ProteinsHistone AcetyltransferasesHistone-Lysine N-MethyltransferaseHistonesLysinemof protein, DrosophilaNuclear ProteinsPolycomb-Group ProteinsPositive Transcriptional Elongation Factor BRNA Polymerase IITip60 protein, DrosophilaTranscriptional Elongation FactorsTranscription Factors

Identifiers

PMID24244179
PMCPMC3820749
OpenAlexW2077284520

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.