Evidence map›Paper›PMID 27708416›Full record

ArticleScientific reports2016

Loss of Atg16 delays the alcohol-induced sedation response via regulation of Corazonin neuropeptide production in Drosophila.

Kata Varga, Péter Nagy, Katarina Arsikin Csordás, Attila L Kovács, Krisztina Hegedűs, Gábor Juhász

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

22 citing papers in PubMed, 41 citations in OpenAlex.

  1. Molecular mechanism on autophagy associated cardiovascular dysfunction inFrontiers in cell and developmental biology · 2025
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  6. Toxics · 2023
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  9. Autophagy controlsFrontiers in cell and developmental biology · 2022
    Article
  10. Article
  11. Review
  12. Article
  13. GnRH-Related Neurohormones in the Fruit FlyInternational journal of molecular sciences · 2021
    Review
  14. Maternal GABAergic and GnRH/corazonin pathway modulates egg diapause phenotype of the silkwormProceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  15. Review
  16. On the Fly: Recent Progress on Autophagy and Aging in Drosophila.Frontiers in cell and developmental biology · 2019
    Review
  17. Review
  18. A Fly's Eye View of Natural and Drug Reward.Frontiers in physiology · 2018
    Review
  19. UsingBioMed research international · 2018
    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

6 authors at 2 institutions in 1 country.

Kata VargaDepartment of Anatomy, Cell and Developmental Biology, Eötvös Loránd University, Pázmány s. 1/C, Budapest, H-1117 Hungary.
Péter NagyDepartment of Anatomy, Cell and Developmental Biology, Eötvös Loránd University, Pázmány s. 1/C, Budapest, H-1117 Hungary.
Katarina Arsikin CsordásDepartment of Anatomy, Cell and Developmental Biology, Eötvös Loránd University, Pázmány s. 1/C, Budapest, H-1117 Hungary.
Attila L KovácsDepartment of Anatomy, Cell and Developmental Biology, Eötvös Loránd University, Pázmány s. 1/C, Budapest, H-1117 Hungary.
Krisztina HegedűsDepartment of Anatomy, Cell and Developmental Biology, Eötvös Loránd University, Pázmány s. 1/C, Budapest, H-1117 Hungary.
Gábor JuhászDepartment of Anatomy, Cell and Developmental Biology, Eötvös Loránd University, Pázmány s. 1/C, Budapest, H-1117 Hungary.
Eötvös Loránd University · HUHungarian Academy of Sciences · HU

Funding

Wellcome Trust 087518
6 · The paper itself

Abstract

Autophagy defects lead to the buildup of damaged proteins and organelles, reduced survival during starvation and infections, hypersensitivity to stress and toxic substances, and progressive neurodegeneration. Here we show that, surprisingly, Drosophila mutants lacking the core autophagy gene Atg16 are not only defective in autophagy but also exhibit increased resistance to the sedative effects of ethanol, unlike Atg7 or Atg3 null mutant flies. This mutant phenotype is rescued by the re-expression of Atg16 in Corazonin (Crz)-producing neurosecretory cells that are known to promote the sedation response during ethanol exposure, and RNAi knockdown of Atg16 specifically in these cells also delays the onset of ethanol-induced coma. We find that Atg16 and Crz colocalize within these neurosecretory cells, and both Crz protein and mRNA levels are decreased in Atg16 mutant flies. Thus, Atg16 promotes Crz production to ensure a proper organismal sedation response to ethanol.

Indexed as

AnimalsAnimals, Genetically ModifiedAutophagyAutophagy-Related Protein 7Autophagy-Related ProteinsBrainDrosophila melanogasterDrosophila ProteinsEthanolGene DeletionGene Expression RegulationHypnotics and SedativesNeuropeptidesNeurosecretory SystemsProtein IsoformsSignal TransductionAtg16 protein, DrosophilaAtg7 protein, DrosophilaAutophagy-Related Protein 7Autophagy-Related ProteinsCrz protein, DrosophilaDrosophila ProteinsEthanolHypnotics and SedativesNeuropeptidesProtein Isoforms

Identifiers

PMID27708416
PMCPMC5052577
OpenAlexW2528483519

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.