Evidence map›Paper›PMID 26370508›Full record

ArticleMolecular and cellular biology2015

Histone H3 Lysine 36 Trimethylation Is Established over the Xist Promoter by Antisense Tsix Transcription and Contributes to Repressing Xist Expression.

Tatsuya Ohhata, Mika Matsumoto, Martin Leeb, Shinwa Shibata, Satoshi Sakai, Kyoko Kitagawa, Hiroyuki Niida, Masatoshi Kitagawa, Anton Wutz

Open access · hybridAbstract read
In one paragraph

Article in Molecular and cellular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

17 citing papers in PubMed, 33 citations in OpenAlex.

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  17. Deciphering the Epigenetic Code in Embryonic and Dental Pulp Stem Cells.The Yale journal of biology and medicine · 2016
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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

9 authors at 4 institutions in 3 countries.

Tatsuya OhhataDepartment of Molecular Biology, Hamamatsu University School of Medicine, Hamamatsu, Japan WT and MRC Stem Cell Institute, University of Cambridge, Cambridge, United Kingdom.
Mika MatsumotoDepartment of Molecular Biology, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Martin LeebWT and MRC Stem Cell Institute, University of Cambridge, Cambridge, United Kingdom.
Shinwa ShibataDepartment of Stem Cell Biology, Graduate School of Medicine, Kanazawa University, Kanazawa, Japan.
Satoshi SakaiDepartment of Molecular Biology, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Kyoko KitagawaDepartment of Molecular Biology, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Hiroyuki NiidaDepartment of Molecular Biology, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Masatoshi KitagawaDepartment of Molecular Biology, Hamamatsu University School of Medicine, Hamamatsu, Japan kitamasa@hama-med.ac.jp awutz@ethz.ch.
Anton WutzWT and MRC Stem Cell Institute, University of Cambridge, Cambridge, United Kingdom Institute of Molecular Health Sciences, ETH, Zurich, Switzerland kitamasa@hama-med.ac.jp awutz@ethz.ch.
Hamamatsu University School of Medicine · JPWellcome/MRC Cambridge Stem Cell Institute · GBKanazawa University · JPUniversity of Cambridge · GB

Funding

Wellcome Trust 97922
6 · The paper itself

Abstract

One of the two X chromosomes in female mammals is inactivated by the noncoding Xist RNA. In mice, X chromosome inactivation (XCI) is regulated by the antisense RNA Tsix, which represses Xist on the active X chromosome. In the absence of Tsix, PRC2-mediated histone H3 lysine 27 trimethylation (H3K27me3) is established over the Xist promoter. Simultaneous disruption of Tsix and PRC2 leads to derepression of Xist and in turn silencing of the single X chromosome in male embryonic stem cells. Here, we identified histone H3 lysine 36 trimethylation (H3K36me3) as a modification that is recruited by Tsix cotranscriptionally and extends over the Xist promoter. Reduction of H3K36me3 by expression of a mutated histone H3.3 with a substitution of methionine for lysine at position 36 causes a significant derepression of Xist. Moreover, depletion of the H3K36 methylase Setd2 leads to upregulation of Xist, suggesting H3K36me3 as a modification that contributes to the mechanism of Tsix function in regulating XCI. Furthermore, we found that reduction of H3K36me3 does not facilitate an increase in H3K27me3 over the Xist promoter, indicating that additional mechanisms exist by which Tsix blocks PRC2 recruitment to the Xist promoter.

Indexed as

Transcription, GeneticX Chromosome InactivationAnimalsCell LineDown-RegulationFemaleHistonesLysineMaleMethylationMiceMutationPromoter Regions, GeneticRNA, Long NoncodingHistonesLysineRNA, Long NoncodingTsix transcript, mouseXIST non-coding RNA

Identifiers

PMID26370508
PMCPMC4609750
OpenAlexW1830479932

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.