Evidence map›Paper›PMID 26621269›Full record

ArticleBMC biology2015

Loss of Ezh2 promotes a midbrain-to-forebrain identity switch by direct gene derepression and Wnt-dependent regulation.

Martina Zemke, Kalina Draganova, Annika Klug, Anne Schöler, Luis Zurkirchen, Max Hans-Peter Gay, Phil Cheng, Haruhiko Koseki, Tomas Valenta, Dirk Schübeler and 2 more

Open access · goldAbstract read
In one paragraph

Article in BMC biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.2field-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

26 citing papers in PubMed, 42 citations in OpenAlex.

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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

12 authors at 4 institutions in 2 countries.

Martina ZemkeInstitute of Anatomy, University of Zürich, Zürich, Switzerland. martina.zemke@anatom.uzh.ch.
Kalina DraganovaInstitute of Anatomy, University of Zürich, Zürich, Switzerland. kalina.draganova@helmholtz-muenchen.de.
Annika KlugInstitute of Anatomy, University of Zürich, Zürich, Switzerland. annika.klug@uzh.ch.
Anne SchölerFriedrich Miescher Institute for Biomedical Research, Basel, Switzerland. anne.schoeler@helmholtz-muenchen.de.
Luis ZurkirchenInstitute of Anatomy, University of Zürich, Zürich, Switzerland. luis.zurkirchen@uzh.ch.
Max Hans-Peter GayInstitute of Anatomy, University of Zürich, Zürich, Switzerland. max.g@unibas.ch.
Phil ChengDepartment of Dermatology, University Hospital Zurich, Zürich, Switzerland. Phil.Cheng@usz.ch.
Haruhiko KosekiRIKEN Center for Integrative Medical Sciences, RIKEN Yokohama Institute, Yokohama, Japan. koseki@rcai.riken.go.jp.
Tomas ValentaInstitute of Molecular Life Sciences, University of Zürich, Zürich, Switzerland. tomas.valenta@imls.uzh.ch.
Dirk SchübelerFriedrich Miescher Institute for Biomedical Research, Basel, Switzerland. Dirk.Schubeler@fmi.ch.
Konrad BaslerInstitute of Molecular Life Sciences, University of Zürich, Zürich, Switzerland. konrad.basler@imls.uzh.ch.
Lukas SommerInstitute of Anatomy, University of Zürich, Zürich, Switzerland. lukas.sommer@anatom.uzh.ch.
University of Zurich · CHFriedrich Miescher Institute · CHRIKEN Center for Integrative Medical Sciences · JPUniversity Hospital of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPrecise spatiotemporal control of gene expression is essential for the establishment of correct cell numbers and identities during brain development. This process involves epigenetic control mechanisms, such as those mediated by the polycomb group protein Ezh2, which catalyzes trimethylation of histone H3K27 (H3K27me3) and thereby represses gene expression.

resultsHerein, we show that Ezh2 plays a crucial role in the development and maintenance of the midbrain. Conditional deletion of Ezh2 in the developing midbrain resulted in decreased neural progenitor proliferation, which is associated with derepression of cell cycle inhibitors and negative regulation of Wnt/β-catenin signaling. Of note, Ezh2 ablation also promoted ectopic expression of a forebrain transcriptional program involving derepression of the forebrain determinants Foxg1 and Pax6. This was accompanied by reduced expression of midbrain markers, including Pax3 and Pax7, as a consequence of decreased Wnt/β-catenin signaling.

conclusionEzh2 is required for appropriate brain growth and maintenance of regional identity by H3K27me3-mediated gene repression and control of canonical Wnt signaling.

Indexed as

Gene Expression Regulation, DevelopmentalWnt Signaling PathwayAnimalsEnhancer of Zeste Homolog 2 ProteinEpigenesis, GeneticMesencephalonMicePolycomb Repressive Complex 2ProsencephalonEnhancer of Zeste Homolog 2 ProteinEzh2 protein, mousePolycomb Repressive Complex 2

Identifiers

PMID26621269
PMCPMC4665911
OpenAlexW2186697921

What OpenQuestion holds

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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.