Evidence map›Paper›PMID 32060339›Full record

ArticleScientific reports2020

The STING pathway does not contribute to behavioural or mitochondrial phenotypes in Drosophila Pink1/parkin or mtDNA mutator models.

Juliette J Lee, Simonetta Andreazza, Alexander J Whitworth

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

21 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Targeting mitophagy in neurodegenerative diseases.Nature reviews. Drug discovery · 2025
    Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Reduced penetrance of Parkinson's disease models.Medizinische Genetik : Mitteilungsblatt des Berufsverbandes Medizinische Genetik e.V · 2022
    Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Mitochondrial function in development and disease.Disease models & mechanisms · 2021
    Review
  16. The Importance ofCells · 2021
    Review
  17. Review
  18. Review
  19. Review
  20. 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

3 authors at 1 institution in 1 country.

Juliette J LeeMRC Mitochondrial Biology Unit, University of Cambridge, Cambridge Biomedical Campus, Hills Road, Cambridge, CB2 0XY, United Kingdom.ORCID http://orcid.org/0000-0002-4281-2491
Simonetta AndreazzaMRC Mitochondrial Biology Unit, University of Cambridge, Cambridge Biomedical Campus, Hills Road, Cambridge, CB2 0XY, United Kingdom.ORCID http://orcid.org/0000-0001-8816-4955
Alexander J WhitworthMRC Mitochondrial Biology Unit, University of Cambridge, Cambridge Biomedical Campus, Hills Road, Cambridge, CB2 0XY, United Kingdom. a.whitworth@mrc-mbu.cam.ac.uk.ORCID http://orcid.org/0000-0002-1154-6629
University of Cambridge · GB

Funding

Resource Component: Acquisition, maintenance and distribution of Drosophila stocksP40OD018537 · OD · TRUSTEES OF INDIANA UNIVERSITY · PI Annette L. Parks · 2014 to 2026
$13.5M
Medical Research Council MC_UP_1501/1Medical Research Council MC_UU_00015/4Medical Research Council MC_UU_00015/6NIH HHS P40 OD018537
6 · The paper itself

Abstract

Mutations in PINK1 and Parkin/PRKN cause the degeneration of dopaminergic neurons in familial forms of Parkinson's disease but the precise pathogenic mechanisms are unknown. The PINK1/Parkin pathway has been described to play a central role in mitochondrial homeostasis by signalling the targeted destruction of damaged mitochondria, however, how disrupting this process leads to neuronal death was unclear until recently. An elegant study in mice revealed that the loss of Pink1 or Prkn coupled with an additional mitochondrial stress resulted in the aberrant activation of the innate immune signalling, mediated via the cGAS/STING pathway, causing degeneration of dopaminergic neurons and motor impairment. Genetic knockout of Sting was sufficient to completely prevent neurodegeneration and accompanying motor deficits. To determine whether Sting plays a conserved role in Pink1/parkin related pathology, we tested for genetic interactions between Sting and Pink1/parkin in Drosophila. Surprisingly, we found that loss of Sting, or its downstream effector Relish, was insufficient to suppress the behavioural deficits or mitochondria disruption in the Pink1/parkin mutants. Thus, we conclude that phenotypes associated with loss of Pink1/parkin are not universally due to aberrant activation of the STING pathway.

Indexed as

AnimalsBehavior, AnimalDisease Models, AnimalDNA, MitochondrialDopaminergic NeuronsDrosophila melanogasterDrosophila ProteinsHumansMembrane ProteinsMiceMitochondriaParkinson DiseasePhenotypeProtein Serine-Threonine KinasesPTEN-Induced Putative KinaseSignal TransductionDNA, MitochondrialDrosophila ProteinsMembrane Proteinspark protein, DrosophilaPINK1 protein, DrosophilaProtein Serine-Threonine KinasesPTEN-Induced Putative KinaseSTING ProteinSting protein, DrosophilaUbiquitin-Protein Ligases

Identifiers

PMID32060339
PMCPMC7021792
OpenAlexW3006459452

What OpenQuestion holds

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LicenceCC BY
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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.