Evidence map›Paper›PMID 24137011›Full record

ArticleNucleic acids research2014

The ADAR RNA editing enzyme controls neuronal excitability in Drosophila melanogaster.

Xianghua Li, Ian M Overton, Richard A Baines, Liam P Keegan, Mary A O'Connell

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

20 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
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  13. Review
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  15. ADAR RNA editing below the backbone.RNA (New York, N.Y.) · 2017
    Review
  16. CircRNAs in the brain.RNA biology · 2017
    Review
  17. Article
  18. Article
  19. Review
  20. 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

5 authors at 4 institutions in 2 countries.

Xianghua LiMRC Human Genetics Unit, Institute of Genetics and Molecular Medicine at the University of Edinburgh, Crewe Road, Edinburgh EH4 2XU, Scotland, UK, Faculty of Life Sciences, University of Manchester, Oxford Road, Manchester M13 9PT, UK and Department of Molecular Biosciences, The Wenner Gren Institute, Stockholm University, Svante Arrhenius väg 20C, 106 91 Stockholm, Sweden.
Ian M Overton
Richard A Baines
Liam P Keegan
Mary A O'Connell
Institute of Genetics and Cancer · GBStockholm University · SEUniversity of Edinburgh · GBUniversity of Manchester · GB

Funding

Medical Research Council MC_PC_U127584490Medical Research Council MC_U127584490
6 · The paper itself

Abstract

RNA editing by deamination of specific adenosine bases to inosines during pre-mRNA processing generates edited isoforms of proteins. Recoding RNA editing is more widespread in Drosophila than in vertebrates. Editing levels rise strongly at metamorphosis, and Adar(5G1) null mutant flies lack editing events in hundreds of CNS transcripts; mutant flies have reduced viability, severely defective locomotion and age-dependent neurodegeneration. On the other hand, overexpressing an adult dADAR isoform with high enzymatic activity ubiquitously during larval and pupal stages is lethal. Advantage was taken of this to screen for genetic modifiers; Adar overexpression lethality is rescued by reduced dosage of the Rdl (Resistant to dieldrin), gene encoding a subunit of inhibitory GABA receptors. Reduced dosage of the Gad1 gene encoding the GABA synthetase also rescues Adar overexpression lethality. Drosophila Adar(5G1) mutant phenotypes are ameliorated by feeding GABA modulators. We demonstrate that neuronal excitability is linked to dADAR expression levels in individual neurons; Adar-overexpressing larval motor neurons show reduced excitability whereas Adar(5G1) null mutant or targeted Adar knockdown motor neurons exhibit increased excitability. GABA inhibitory signalling is impaired in human epileptic and autistic conditions, and vertebrate ADARs may have a relevant evolutionarily conserved control over neuronal excitability.

Indexed as

Action PotentialsAdenosine DeaminaseAnimalsChromosomes, InsectDrosophila melanogasterDrosophila Proteinsgamma-Aminobutyric AcidGenes, LethalGenotypeLarvaMotor NeuronsPhenotypeReceptors, GABA-ARNA EditingSignal TransductionAdar protein, DrosophilaAdenosine DeaminaseDrosophila Proteinsgamma-Aminobutyric AcidRdl protein, DrosophilaReceptors, GABA-A

Identifiers

PMID24137011
PMCPMC3902911
OpenAlexW2118402518

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.