Evidence map›Paper›PMID 23167977›Full record

ArticleNeural development2012

Schwann cell myelination requires Dynein function.

Melissa M Langworthy, Bruce Appel

Abstract read
In one paragraph

Article in Neural development, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–field-weighted citation impact
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

18 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Dynein/dynactin is necessary for anterograde transport ofProceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  10. Review
  11. Article
  12. Fbxw7 Limits Myelination by Inhibiting mTOR Signaling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
  13. Article
  14. Review
  15. CNS myelination requires cytoplasmic dynein function.Developmental dynamics : an official publication of the American Association of Anatomists · 2015
    Article
  16. Article
  17. Article
  18. 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

2 authors.

Melissa M LangworthyDepartment of Pediatrics, University of Colorado School of Medicine, MS 8108, Aurora, CO, 80045, USA.
Bruce Appel

Funding

ZEBRAFISH INTERNATIONAL RESOURCE CENTERP40RR012546 · NCRR · UNIVERSITY OF OREGON · PI WESTERFIELD, MONTE · 1998 to 2011
$21.9M
ZEBRAFISH TRANSGENIC CORE - ROCKY MOUNTAIN NEUROLOGICAL DISORDERS CORE CENTERP30NS048154 · NINDS · UNIVERSITY OF COLORADO DENVER · PI RIBERA, ANGELES BADELL · 2004 to 2020
$10.1M
Genetic Analysis of Peripheral Nerve DevelopmentR01NS062717 · NINDS · UNIVERSITY OF COLORADO DENVER · PI APPEL, BRUCE H · 2009 to 2013
$1.6M
NCRR NIH HHS P40 RR012546NINDS NIH HHS P30 NS048154NINDS NIH HHS R01 NS062717
6 · The paper itself

Abstract

backgroundInteraction of Schwann cells with axons triggers signal transduction that drives expression of Pou3f1 and Egr2 transcription factors, which in turn promote myelination. Signal transduction appears to be mediated, at least in part, by cyclic adenosine monophosphate (cAMP) because elevation of cAMP levels can stimulate myelination in the absence of axon contact. The mechanisms by which the myelinating signal is conveyed remain unclear.

resultsBy analyzing mutations that disrupt myelination in zebrafish, we learned that Dynein cytoplasmic 1 heavy chain 1 (Dync1h1), which functions as a motor for intracellular molecular trafficking, is required for peripheral myelination. In dync1h1 mutants, Schwann cell progenitors migrated to peripheral nerves but then failed to express Pou3f1 and Egr2 or make myelin membrane. Genetic mosaic experiments revealed that robust Myelin Basic Protein expression required Dync1h1 function within both Schwann cells and axons. Finally, treatment of dync1h1 mutants with a drug to elevate cAMP levels stimulated myelin gene expression.

conclusionDync1h1 is required for retrograde transport in axons and mutations of Dync1h1 have been implicated in axon disease. Our data now provide evidence that Dync1h1 is also required for efficient myelination of peripheral axons by Schwann cells, perhaps by facilitating signal transduction necessary for myelination.

Indexed as

AnimalsAnimals, Genetically ModifiedCell DifferentiationCell MovementCentral Nervous SystemColforsinCyclic AMPCytoplasmic DyneinsDemyelinating DiseasesEmbryo, NonmammalianGene Expression Regulation, DevelopmentalGreen Fluorescent ProteinsLarvaMicroscopy, Electron, TransmissionMorpholinosMutationColforsinCyclic AMPCytoplasmic DyneinsDYNC1H1 protein, zebrafishGreen Fluorescent ProteinsMorpholinosMyelin Basic ProteinRNAZebrafish Proteins

Identifiers

PMID23167977
PMCPMC3520773

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.