Evidence map›Paper›PMID 32161768›Full record

ArticleMicrobial cell (Graz, Austria)2020

The euchromatic histone mark H3K36me3 preserves heterochromatin through sequestration of an acetyltransferase complex in fission yeast.

Paula R Georgescu, Matías Capella, Sabine Fischer-Burkart, Sigurd Braun

Open access · goldAbstract read
In one paragraph

Article in Microbial cell (Graz, Austria), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

16 citing papers in PubMed, 26 citations in OpenAlex.

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  8. Frontiers in epigenetics and epigenomics · 2024
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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

4 authors at 1 institution in 1 country.

Paula R GeorgescuDepartment of Physiological Chemistry, BioMedical Center (BMC), Ludwig-Maximilians-Universität München, Martinsried, Germany.
Matías CapellaDepartment of Physiological Chemistry, BioMedical Center (BMC), Ludwig-Maximilians-Universität München, Martinsried, Germany.
Sabine Fischer-BurkartDepartment of Physiological Chemistry, BioMedical Center (BMC), Ludwig-Maximilians-Universität München, Martinsried, Germany.
Sigurd BraunDepartment of Physiological Chemistry, BioMedical Center (BMC), Ludwig-Maximilians-Universität München, Martinsried, Germany.
Ludwig-Maximilians-Universität München · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Maintaining the identity of chromatin states requires mechanisms that ensure their structural integrity through the concerted actions of histone modifiers, readers, and erasers. Histone H3K9me and H3K27me are hallmarks of repressed heterochromatin, whereas H3K4me and H3K36me are associated with actively transcribed euchromatin. Paradoxically, several studies have reported that loss of Set2, the methyltransferase responsible for H3K36me, causes de-repression of heterochromatin. Here we show that unconstrained activity of the acetyltransferase complex Mst2C, which antagonizes heterochromatin, is the main cause of the silencing defects observed in Set2-deficient cells. As previously shown, Mst2C is sequestered to actively transcribed chromatin via binding to H3K36me3 that is recognized by the PWWP domain protein Pdp3. We demonstrate that combining deletions of

Indexed as

acetyltransferasechromatinheterochromatinhistone modificationsilencing

Identifiers

PMID32161768
PMCPMC7052950
OpenAlexW3007032106

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.