Evidence map›Paper›PMID 24952591›Full record

ArticleMolecular systems biology2014

Screen for mitochondrial DNA copy number maintenance genes reveals essential role for ATP synthase.

Atsushi Fukuoh, Giuseppe Cannino, Mike Gerards, Suzanne Buckley, Selena Kazancioglu, Filippo Scialo, Eero Lihavainen, Andre Ribeiro, Eric Dufour, Howard T Jacobs

Open access · goldAbstract read
In one paragraph

Article in Molecular systems biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

32 citing papers in PubMed, 59 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Mitochondrial DNA: cellular genotoxic stress sentinel.Trends in biochemical sciences · 2021
    Review
  13. Review
  14. Article
  15. Mrx6 regulates mitochondrial DNA copy number inMolecular biology of the cell · 2020
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  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

10 authors at 3 institutions in 2 countries.

Atsushi FukuohBioMediTech and Tampere University Hospital, University of Tampere, Tampere, Finland Department of Clinical Chemistry and Laboratory Medicine, Kyushu University Graduate school of Medical Sciences, Fukuoka, Japan Department of Medical Laboratory Science, Junshin Gakuen University, Fukuoka, Japan.
Giuseppe CanninoBioMediTech and Tampere University Hospital, University of Tampere, Tampere, Finland.
Mike GerardsBioMediTech and Tampere University Hospital, University of Tampere, Tampere, Finland.
Suzanne BuckleyBioMediTech and Tampere University Hospital, University of Tampere, Tampere, Finland.
Selena KazanciogluBioMediTech and Tampere University Hospital, University of Tampere, Tampere, Finland.
Filippo ScialoBioMediTech and Tampere University Hospital, University of Tampere, Tampere, Finland.
Eero LihavainenDepartment of Signal Processing, Tampere University of Technology, Tampere, Finland.
Andre RibeiroDepartment of Signal Processing, Tampere University of Technology, Tampere, Finland.
Eric DufourBioMediTech and Tampere University Hospital, University of Tampere, Tampere, Finland.
Howard T JacobsBioMediTech and Tampere University Hospital, University of Tampere, Tampere, Finland Research Program of Molecular Neurology, University of Helsinki, Helsinki, Finland howard.t.jacobs@uta.fi.
Tampere University · FITampere University Hospital · FIJunshin Gakuen University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The machinery of mitochondrial DNA (mtDNA) maintenance is only partially characterized and is of wide interest due to its involvement in disease. To identify novel components of this machinery, plus other cellular pathways required for mtDNA viability, we implemented a genome-wide RNAi screen in Drosophila S2 cells, assaying for loss of fluorescence of mtDNA nucleoids stained with the DNA-intercalating agent PicoGreen. In addition to previously characterized components of the mtDNA replication and transcription machineries, positives included many proteins of the cytosolic proteasome and ribosome (but not the mitoribosome), three proteins involved in vesicle transport, some other factors involved in mitochondrial biogenesis or nuclear gene expression, > 30 mainly uncharacterized proteins and most subunits of ATP synthase (but no other OXPHOS complex). ATP synthase knockdown precipitated a burst of mitochondrial ROS production, followed by copy number depletion involving increased mitochondrial turnover, not dependent on the canonical autophagy machinery. Our findings will inform future studies of the apparatus and regulation of mtDNA maintenance, and the role of mitochondrial bioenergetics and signaling in modulating mtDNA copy number.

Indexed as

Genes, EssentialAnimalsAutophagyCell LineDNA, MitochondrialDrosophila melanogasterDrosophila ProteinsGene DosageGene Expression RegulationGene LibraryGenomeMitochondrial Proton-Translocating ATPasesReactive Oxygen SpeciesRNA InterferenceDNA, MitochondrialDrosophila ProteinsMitochondrial Proton-Translocating ATPasesReactive Oxygen Speciescomplex VDNA replicationmitochondrial biogenesismitochondrial DNAmitophagynucleasenucleoidreactive oxygen species

Identifiers

PMID24952591
PMCPMC4265055
OpenAlexW2160824763

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.