Evidence map›Paper›PMID 27588417›Full record

ArticlePLoS genetics2016

dBRWD3 Regulates Tissue Overgrowth and Ectopic Gene Expression Caused by Polycomb Group Mutations.

Hsueh-Tzu Shih, Wei-Yu Chen, Kwei-Yan Liu, Zong-Siou Shih, Yi-Jyun Chen, Paul-Chen Hsieh, Kuan-Lin Kuo, Kuo-How Huang, Pang-Hung Hsu, Ya-Wen Liu and 4 more

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In one paragraph

Article in PLoS genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. BRWD3 promotes KDM5 degradation to maintain H3K4 methylation levels.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  2. BRWD3 promotes KDM5 degradation to maintain H3K4 methylation levels.bioRxiv : the preprint server for biology · 2023
    Article
  3. Article
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.

Hsueh-Tzu ShihInstitute of Molecular Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan.
Wei-Yu ChenInstitute of Molecular Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan.
Kwei-Yan LiuInstitute of Molecular Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan.
Zong-Siou ShihInstitute of Molecular Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan.
Yi-Jyun ChenInstitute of Molecular Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan.
Paul-Chen HsiehDepartment of Anatomical Pathology, Far Eastern Memorial Hospital, New Taipei City, Taiwan.
Kuan-Lin KuoGraduate Institute of Toxicology, National Taiwan University College of Medicine, Taipei, Taiwan.
Kuo-How HuangDepartment of Urology, National Taiwan University College of Medicine and Hospital, Taipei, Taiwan.
Pang-Hung HsuDepartment of Bioscience and Biotechnology, National Taiwan Ocean University, Keelung, Taiwan.
Ya-Wen LiuInstitute of Molecular Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan.
Shih-Peng ChanGraduate Institute of Microbiology, College of Medicine, National Taiwan University, Taipei, Taiwan.ORCID 0000-0001-6322-2821
Hsiu-Hsiang LeeInstitute of Molecular Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan.ORCID 0000-0001-7707-8461
Yu-Chen TsaiDepartment of Life Science and Life Science Center, Tunghai University, Taichung, Taiwan.
June-Tai WuInstitute of Molecular Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To maintain a particular cell fate, a unique set of genes should be expressed while another set is repressed. One way to repress gene expression is through Polycomb group (PcG) proteins that compact chromatin into a silent configuration. In addition to cell fate maintenance, PcG proteins also maintain normal cell physiology, for example cell cycle. In the absence of PcG, ectopic activation of the PcG-repressed genes leads to developmental defects and malignant tumors. Little is known about the molecular nature of ectopic gene expression; especially what differentiates expression of a given gene in the orthotopic tissue (orthotopic expression) and the ectopic expression of the same gene due to PcG mutations. Here we present that ectopic gene expression in PcG mutant cells specifically requires dBRWD3, a negative regulator of HIRA/Yemanuclein (YEM)-mediated histone variant H3.3 deposition. dBRWD3 mutations suppress both the ectopic gene expression and aberrant tissue overgrowth in PcG mutants through a YEM-dependent mechanism. Our findings identified dBRWD3 as a critical regulator that is uniquely required for ectopic gene expression and aberrant tissue overgrowth caused by PcG mutations.

Indexed as

AnimalsCell CycleCell Cycle ProteinsCell DifferentiationChromatinDNA-Binding ProteinsDrosophila melanogasterDrosophila ProteinsEyeGene Expression Regulation, DevelopmentalHistone ChaperonesHistonesImaginal DiscsMutationNuclear ProteinsPolycomb-Group ProteinsBRWD3 protein, DrosophilaCell Cycle ProteinsChromatinDNA-Binding ProteinsDrosophila ProteinsHira protein, DrosophilaHistone ChaperonesHistonesNuclear ProteinsPolycomb-Group ProteinsTranscription Factorsyem protein, Drosophila

Identifiers

PMID27588417
PMCPMC5010193

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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.