Evidence map›Paper›PMID 25666827›Full record

ArticleEMBO reports2015

Intellectual disability-associated dBRWD3 regulates gene expression through inhibition of HIRA/YEM-mediated chromatin deposition of histone H3.3.

Wei-Yu Chen, Hsueh-Tzu Shih, Kwei-Yan Liu, Zong-Siou Shih, Li-Kai Chen, Tsung-Han Tsai, Mei-Ju Chen, Hsuan Liu, Bertrand Chin-Ming Tan, Chien-Yu Chen and 4 more

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in EMBO reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed, 22 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 4 institutions in 2 countries.

Wei-Yu ChenInstitute of Molecular Medicine College of Medicine National Taiwan University, Taipei, Taiwan.
Hsueh-Tzu ShihInstitute 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.
Li-Kai ChenInstitute of Molecular Medicine College of Medicine National Taiwan University, Taipei, Taiwan.
Tsung-Han TsaiInstitute of Molecular Medicine College of Medicine National Taiwan University, Taipei, Taiwan.
Mei-Ju ChenGenome and Systems Biology Degree Program, National Taiwan University and Academia Sinica, Taipei, Taiwan.
Hsuan LiuDepartment of Cell and Molecular Biology, College of Medicine Chang Gung University, Tao-Yuan, Taiwan Molecular Medicine Research Center Chang Gung University, Tao-Yuan, Taiwan.
Bertrand Chin-Ming TanMolecular Medicine Research Center Chang Gung University, Tao-Yuan, Taiwan Department of Biomedical Sciences and Graduate Institute of Biomedical Sciences, College of Medicine Chang Gung University, Tao-Yuan, Taiwan.
Chien-Yu ChenBio-Industrial Mechatronics Engineering, National Taiwan University, Taipei, Taiwan.
Hsiu-Hsiang LeeInstitute of Molecular Medicine College of Medicine National Taiwan University, Taipei, Taiwan.
Benjamin LoppinCentre de Génétique et de Physiologie Moléculaire et Cellulaire CNRS UMR5534 Université Claude Bernard Lyon 1, Villeurbanne, France.
Ounissa Aït-AhmedInstitute of Regenerative medicine and Biotherapy (IRMB) Inserm U1203 Saint-Eloi Hospital, CHRU Montpellier, France.
June-Tai WuInstitute of Molecular Medicine College of Medicine National Taiwan University, Taipei, Taiwan Department of Dermatology, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei, Taiwan Research Center for Developmental Biology and Regenerative Medicine National Taiwan University, Taipei, Taiwan junetai.wu@gmail.com.
National Taiwan University · TWChang Gung University · TWInserm · FRUniversité Claude Bernard Lyon 1 · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Many causal mutations of intellectual disability have been found in genes involved in epigenetic regulations. Replication-independent deposition of the histone H3.3 variant by the HIRA complex is a prominent nucleosome replacement mechanism affecting gene transcription, especially in postmitotic neurons. However, how HIRA-mediated H3.3 deposition is regulated in these cells remains unclear. Here, we report that dBRWD3, the Drosophila ortholog of the intellectual disability gene BRWD3, regulates gene expression through H3.3, HIRA, and its associated chaperone Yemanuclein (YEM), the fly ortholog of mammalian Ubinuclein1. In dBRWD3 mutants, increased H3.3 levels disrupt gene expression, dendritic morphogenesis, and sensory organ differentiation. Inactivation of yem or H3.3 remarkably suppresses the global transcriptome changes and various developmental defects caused by dBRWD3 mutations. Our work thus establishes a previously unknown negative regulation of H3.3 and advances our understanding of BRWD3-dependent intellectual disability.

Indexed as

Gene Expression Regulation, DevelopmentalAnimalsBromodomain Containing ProteinsCell Cycle ProteinsChromatinDNA-Binding ProteinsDrosophila melanogasterDrosophila ProteinsHistone ChaperonesHistonesHumansIntellectual DisabilityMorphogenesisNuclear ProteinsRNA, Small InterferingSequence Homology, Amino AcidBromodomain Containing ProteinsBRWD3 protein, humanCell Cycle ProteinsChromatinDNA-Binding ProteinsDrosophila ProteinsHira protein, DrosophilaHIRA protein, humanHistone ChaperonesHistonesNuclear ProteinsRNA, Small InterferingTranscription FactorsUBN1 protein, humanyem protein, DrosophilaBRWD3HIRAhistone H3.3intellectual disabilityYEM

Identifiers

PMID25666827
PMCPMC4388619
OpenAlexW2152471283

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.