Evidence map›Paper›PMID 20949033›Full record

ArticlePloS one2010

Drosophila Porin/VDAC affects mitochondrial morphology.

Jeehye Park, Yongsung Kim, Sekyu Choi, Hyongjong Koh, Sang-Hee Lee, Jin-Man Kim, Jongkyeong Chung

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 2 pooled it
1.9field-weighted citation impact, top 15% 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

30 citing papers in PubMed, 2 syntheses or guidelines pooled it, 56 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Review
  6. Mitochondrial Differentiation during Spermatogenesis: Lessons fromInternational journal of molecular sciences · 2024
    Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Decision between mitophagy and apoptosis by Parkin via VDAC1 ubiquitination.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Mitochondrial calcium uniporter inThe Journal of biological chemistry · 2017
    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

7 authors at 3 institutions in 1 country.

Jeehye ParkNational Creative Research Initiatives Center for Energy Homeostasis Regulation, Seoul National University, Seoul, Korea.
Yongsung Kim
Sekyu Choi
Hyongjong Koh
Sang-Hee Lee
Jin-Man Kim
Jongkyeong Chung
Seoul National University · KRChungnam National University · KRDong-A University · KR

Funding

Research Training in BiogerontologyT32AG000114 · NIA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SCOTT PLETCHER · 1985 to 2026
$12.4M
NIA NIH HHS T32 AG000114
6 · The paper itself

Abstract

Voltage-dependent anion channel (VDAC) has been suggested to be a mediator of mitochondrial-dependent cell death induced by Ca(2+) overload, oxidative stress and Bax-Bid activation. To confirm this hypothesis in vivo, we generated and characterized Drosophila VDAC (porin) mutants and found that Porin is not required for mitochondrial apoptosis, which is consistent with the previous mouse studies. We also reported a novel physiological role of Porin. Loss of porin resulted in locomotive defects and male sterility. Intriguingly, porin mutants exhibited elongated mitochondria in indirect flight muscle, whereas Porin overexpression produced fragmented mitochondria. Through genetic analysis with the components of mitochondrial fission and fusion, we found that the elongated mitochondria phenotype in porin mutants were suppressed by increased mitochondrial fission, but enhanced by increased mitochondrial fusion. Furthermore, increased mitochondrial fission by Drp1 expression suppressed the flight defects in the porin mutants. Collectively, our study showed that loss of Drosophila Porin results in mitochondrial morphological defects and suggested that the defective mitochondrial function by Porin deficiency affects the mitochondrial remodeling process.

Indexed as

AnimalsDrosophilaImmunohistochemistryMaleMitochondriaMutationSpermatozoaVoltage-Dependent Anion ChannelsVoltage-Dependent Anion Channels

Identifiers

PMID20949033
PMCPMC2951900
OpenAlexW2072921418

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.