Evidence map›Paper›PMID 20592219›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010

Evidence that myosin activity opposes microtubule-based axonal transport of mitochondria.

Divya Pathak, Katharine J Sepp, Peter J Hollenbeck

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
118citing papers in PubMed, 1 pooled it
6.1field-weighted citation impact, top 3% 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

118 citing papers in PubMed, 1 synthesis or guideline pooled it, 191 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. The role of impaired mitochondrial function in neurological manifestations of mitochondrial diseases.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. A novel, rapidly progressive ataxia due to a spontaneous Myo5a mutation in mice impairs transport proteins and alters mitochondria.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  8. Review
  9. Axonal mitophagy in retinal ganglion cells.Cell communication and signaling : CCS · 2024
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. The multiple links between actin and mitochondria.Nature reviews. Molecular cell biology · 2023
    Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

58 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Divya PathakDepartment of Biological Sciences and Purdue University Integrative Neuroscience Program, West Lafayette, IN 47907, USA.
Katharine J Sepp
Peter J Hollenbeck
Harvard University · USPurdue University West Lafayette · US

Funding

CONTROL OF NEURONAL ORGANELLE TRANSPORTR01NS027073 · NINDS · PURDUE UNIVERSITY WEST LAFAYETTE · PI HOLLENBECK, PETER J. · 1990 to 2013
$3.6M
Control of Neural Organelle TransportR56NS027073 · NINDS · PURDUE UNIVERSITY · PI HOLLENBECK, PETER J. · 2009 to 2009
$374k
NINDS NIH HHS NS 27073NINDS NIH HHS R01 NS027073NINDS NIH HHS R56 NS027073
6 · The paper itself

Abstract

Neurons transport and position mitochondria using a combination of saltatory, bidirectional movements and stationary docking. Axonal mitochondria move along microtubules (MTs) using kinesin and dynein motors, but actin and myosin also play a poorly defined role in their traffic. To ascertain this role, we have used RNA interference (RNAi) to deplete specific myosin motors in cultured Drosophila neurons and quantified the effects on mitochondrial motility. We produced a fly strain expressing the Caenorhabditis elegans RNA transporter SID-1 in neurons to increase the efficacy of RNAi in primary cultures. These neurons exhibited significantly increased RNAi-mediated knockdown of gene expression compared with neurons not expressing this transporter. Using this system, we observed a significant increase in mitochondrial transport during myosin V depletion. Mitochondrial mean velocity and duty cycle were augmented in both anterograde and retrograde directions, and the fraction of mitochondrial flux contained in long runs almost doubled for anterograde movement. Myosin VI depletion increased the same movement parameters but was selective for retrograde movement, whereas myosin II depletion produced no phenotype. An additional effect of myosin V depletion was an increase in mitochondrial length. These data indicate that myosin V and VI play related but distinct roles in regulating MT-based mitochondrial movement: they oppose, rather than complement, protracted MT-based movements and perhaps facilitate organelle docking.

Indexed as

AnimalsAnimals, Genetically ModifiedAxonal TransportCaenorhabditis elegansCaenorhabditis elegans ProteinsCells, CulturedDrosophilaGene Knockdown TechniquesMembrane ProteinsMicrotubulesMitochondriaMovementMyosin Heavy ChainsMyosin Type IIMyosin Type VNeuronsCaenorhabditis elegans ProteinsMembrane ProteinsMyosin Heavy ChainsMyosin Type IIMyosin Type Vmyosin VISID-1 protein, C elegans

Identifiers

PMID20592219
PMCPMC2904968
OpenAlexW2128871447

What OpenQuestion holds

Textmetadata
LicenceTDM
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.