Evidence map›Paper›PMID 19924234›Full record

ArticlePloS one2009

Disruption of mitochondrial DNA replication in Drosophila increases mitochondrial fast axonal transport in vivo.

Rehan M Baqri, Brittany A Turner, Mary B Rheuben, Bradley D Hammond, Laurie S Kaguni, Kyle E Miller

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

19 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. High Dietary Fat Consumption Impairs Axonal Mitochondrial FunctionThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
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  12. The dynamics of the mitochondrial organelle as a potential therapeutic target.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2013
    Review
  13. Review
  14. The axonal transport of mitochondria.Journal of cell science · 2012
    Review
  15. Article
  16. Review
  17. Review
  18. Review
  19. 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.

Rehan M BaqriDepartment of Zoology, Michigan State University, East Lansing, Michigan, USA.
Brittany A Turner
Mary B Rheuben
Bradley D Hammond
Laurie S Kaguni
Kyle E Miller
Michigan State University · USMichigan United · US

Funding

Mitochondrial DNA Replisome: Mechanism, Structure and PhysiologyR01GM045295 · NIGMS · MICHIGAN STATE UNIVERSITY · PI KAGUNI, LAURIE SIMON · 1991 to 2013
$4.0M
NIGMS NIH HHS GM45295NIGMS NIH HHS R01 GM045295
6 · The paper itself

Abstract

Mutations in mitochondrial DNA polymerase (pol gamma) cause several progressive human diseases including Parkinson's disease, Alper's syndrome, and progressive external ophthalmoplegia. At the cellular level, disruption of pol gamma leads to depletion of mtDNA, disrupts the mitochondrial respiratory chain, and increases susceptibility to oxidative stress. Although recent studies have intensified focus on the role of mtDNA in neuronal diseases, the changes that take place in mitochondrial biogenesis and mitochondrial axonal transport when mtDNA replication is disrupted are unknown. Using high-speed confocal microscopy, electron microscopy and biochemical approaches, we report that mutations in pol gamma deplete mtDNA levels and lead to an increase in mitochondrial density in Drosophila proximal nerves and muscles, without a noticeable increase in mitochondrial fragmentation. Furthermore, there is a rise in flux of bidirectional mitochondrial axonal transport, albeit with slower kinesin-based anterograde transport. In contrast, flux of synaptic vesicle precursors was modestly decreased in pol gamma-alpha mutants. Our data indicate that disruption of mtDNA replication does not hinder mitochondrial biogenesis, increases mitochondrial axonal transport, and raises the question of whether high levels of circulating mtDNA-deficient mitochondria are beneficial or deleterious in mtDNA diseases.

Indexed as

DNA ReplicationAnimalsAxonsDNADNA, MitochondrialDrosophilaGreen Fluorescent ProteinsImage Processing, Computer-AssistedImmunohistochemistryKinesinsMicroscopy, ConfocalMicroscopy, ElectronMutationOrganic ChemicalsDNADNA, MitochondrialGreen Fluorescent ProteinsKinesinsOrganic ChemicalsPicoGreen

Identifiers

PMID19924234
PMCPMC2773408
OpenAlexW2046587261

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.