Evidence map›Paper›PMID 26166299›Full record

ArticleDevelopmental cell2015

Actin filament turnover drives leading edge growth during myelin sheath formation in the central nervous system.

Schanila Nawaz, Paula Sánchez, Sebastian Schmitt, Nicolas Snaidero, Mišo Mitkovski, Caroline Velte, Bastian R Brückner, Ioannis Alexopoulos, Tim Czopka, Sang Y Jung and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in Developmental cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 149 papers.

0numbers the graph read from it
0cells of the map it votes in
149citing papers in PubMed
10.7field-weighted citation impact, top 1% 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

149 citing papers in PubMed, 238 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Actin disassembly triggers CNS myelin compaction and wrapping.bioRxiv : the preprint server for biology · 2026
    Article
  8. Article
  9. Article
  10. Mechanobiology of Myelin Generation/Regeneration in Health and Disease.Results and problems in cell differentiation · 2026
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. TMEM63A, associated with hypomyelinating leukodystrophies, is an evolutionarily conserved regulator of myelination.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  17. Review
  18. Article
  19. Article
  20. Article

89 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

16 authors at 5 institutions in 2 countries.

Schanila Nawaz *Max Planck Institute for Experimental Medicine, 37075 Göttingen, Germany.
Paula Sánchez *Max Planck Institute for Experimental Medicine, 37075 Göttingen, Germany.
Sebastian SchmittMax Planck Institute for Experimental Medicine, 37075 Göttingen, Germany.
Nicolas SnaideroMax Planck Institute for Experimental Medicine, 37075 Göttingen, Germany.
Mišo MitkovskiMax Planck Institute for Experimental Medicine, 37075 Göttingen, Germany.
Caroline VelteMax Planck Institute for Experimental Medicine, 37075 Göttingen, Germany.
Bastian R BrücknerInstitute for Physical Chemistry, University of Göttingen, 37075 Göttingen, Germany.
Ioannis AlexopoulosMax Planck Institute for Experimental Medicine, 37075 Göttingen, Germany.
Tim CzopkaCentre for Neuroregeneration, Chancellor's Building, GU 507B, 49 Little France Crescent, Edinburgh, EH16 4SB, UK.
Sang Y JungMax Planck Institute for Experimental Medicine, 37075 Göttingen, Germany.
Jeong S RheeMax Planck Institute for Experimental Medicine, 37075 Göttingen, Germany.
Andreas JanshoffInstitute for Physical Chemistry, University of Göttingen, 37075 Göttingen, Germany.
Walter WitkeInstitute of Genetics, University of Bonn, Karlrobert-Kreiten Strasse 13, 53115 Bonn, Germany.
Iwan A T SchaapIII. Physics Institute, Faculty of Physics, University of Göttingen, 37077 Göttingen, Germany.
David A LyonsCentre for Neuroregeneration, Chancellor's Building, GU 507B, 49 Little France Crescent, Edinburgh, EH16 4SB, UK.
Mikael SimonsMax Planck Institute for Experimental Medicine, 37075 Göttingen, Germany.
Max Planck Institute of Experimental Medicine · DENanoscale Microscopy and Molecular Physiology of the Brain Cluster of Excellence 171 — DFG Research Center 103 · DEUniversity of Edinburgh · GBUniversity of Göttingen · DEUniversity of Bonn · DE

Funding

Wellcome Trust 102836Wellcome Trust 102836/Z/13/Z
6 · The paper itself

Abstract

During CNS development, oligodendrocytes wrap their plasma membrane around axons to generate multilamellar myelin sheaths. To drive growth at the leading edge of myelin at the interface with the axon, mechanical forces are necessary, but the underlying mechanisms are not known. Using an interdisciplinary approach that combines morphological, genetic, and biophysical analyses, we identified a key role for actin filament network turnover in myelin growth. At the onset of myelin biogenesis, F-actin is redistributed to the leading edge, where its polymerization-based forces push out non-adhesive and motile protrusions. F-actin disassembly converts protrusions into sheets by reducing surface tension and in turn inducing membrane spreading and adhesion. We identified the actin depolymerizing factor ADF/cofilin1, which mediates high F-actin turnover rates, as an essential factor in this process. We propose that F-actin turnover is the driving force in myelin wrapping by regulating repetitive cycles of leading edge protrusion and spreading.

Indexed as

Actin CytoskeletonActinsAnimalsAxonsCell AdhesionCell MembraneCells, CulturedCentral Nervous SystemCofilin 1DestrinLuminescent ProteinsMiceMice, Inbred C57BLMice, KnockoutMyelin SheathOligodendrogliaActinsCfl1 protein, mouseCofilin 1DestrinDstn protein, mouseLuminescent ProteinsRed Fluorescent Protein

Identifiers

PMID26166299
PMCPMC4736019
OpenAlexW1839988640

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.