Evidence map›Paper›PMID 25184680›Full record

ArticleGenes & development2014

Double-bromo and extraterminal (BET) domain proteins regulate dendrite morphology and mechanosensory function.

Joshua A Bagley, Zhiqiang Yan, Wei Zhang, Jill Wildonger, Lily Yeh Jan, Yuh Nung Jan

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Genes & development, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

  1. Article
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  5. Zebrafish ParalogsJournal of developmental biology · 2021
    Article
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  12. Manipulation of the host protein acetylation network by human immunodeficiency virus type 1.Critical reviews in biochemistry and molecular biology · 2015
    Review
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

6 authors.

Joshua A BagleyNeuroscience Graduate Program, University of California at San Francisco, San Francisco, California 94158, USA; Howard Hughes Medical Institute, Department of Physiology, Department of Biochemistry and Biophysics, University of California at San Francisco at San Francisco, California 94158, USA.
Zhiqiang YanHoward Hughes Medical Institute, Department of Physiology, Department of Biochemistry and Biophysics, University of California at San Francisco at San Francisco, California 94158, USA.
Wei ZhangHoward Hughes Medical Institute, Department of Physiology, Department of Biochemistry and Biophysics, University of California at San Francisco at San Francisco, California 94158, USA.
Jill WildongerHoward Hughes Medical Institute, Department of Physiology, Department of Biochemistry and Biophysics, University of California at San Francisco at San Francisco, California 94158, USA.
Lily Yeh JanHoward Hughes Medical Institute, Department of Physiology, Department of Biochemistry and Biophysics, University of California at San Francisco at San Francisco, California 94158, USA yuhnung.jan@ucsf.edu.
Yuh Nung JanHoward Hughes Medical Institute, Department of Physiology, Department of Biochemistry and Biophysics, University of California at San Francisco at San Francisco, California 94158, USA yuhnung.jan@ucsf.edu.

Funding

Genetic Dissection of Dendrite DevelopmentR37NS040929 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI JAN, YUH NUNG · 2010 to 2016
$2.5M
Howard Hughes Medical InstituteNINDS NIH HHS R37 NS040929NINDS NIH HHS R37NS040929
6 · The paper itself

Abstract

A complex array of genetic factors regulates neuronal dendrite morphology. Epigenetic regulation of gene expression represents a plausible mechanism to control pathways responsible for specific dendritic arbor shapes. By studying the Drosophila dendritic arborization (da) neurons, we discovered a role of the double-bromodomain and extraterminal (BET) family proteins in regulating dendrite arbor complexity. A loss-of-function mutation in the single Drosophila BET protein encoded by female sterile 1 homeotic [fs(1)h] causes loss of fine, terminal dendritic branches. Moreover, fs(1)h is necessary for the induction of branching caused by a previously identified transcription factor, Cut (Ct), which regulates subtype-specific dendrite morphology. Finally, disrupting fs(1)h function impairs the mechanosensory response of class III da sensory neurons without compromising the expression of the ion channel NompC, which mediates the mechanosensitive response. Thus, our results identify a novel role for BET family proteins in regulating dendrite morphology and a possible separation of developmental pathways specifying neural cell morphology and ion channel expression. Since the BET proteins are known to bind acetylated histone tails, these results also suggest a role of epigenetic histone modifications and the "histone code," in regulating dendrite morphology.

Indexed as

AnimalsDendritesDrosophila melanogasterDrosophila ProteinsEpigenesis, GeneticGene Expression Regulation, DevelopmentalHomeodomain ProteinsHumansMutationNuclear ProteinsProtein BindingProtein Structure, TertiarySensory Receptor CellsTranscription Factorsct protein, DrosophilaDrosophila Proteinsfs(1)h protein, DrosophilaHomeodomain ProteinsNuclear ProteinsTranscription Factorsdendrite morphogenesisdouble bromodomain and extraterminalepigeneticsfemale sterile 1 homeotichistone acetylationmechanosensory function

Identifiers

PMID25184680
PMCPMC4197945

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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.