Evidence map›Paper›PMID 27504968›Full record

ArticleeLife2016

Septin/anillin filaments scaffold central nervous system myelin to accelerate nerve conduction.

Julia Patzig, Michelle S Erwig, Stefan Tenzer, Kathrin Kusch, Payam Dibaj, Wiebke Möbius, Sandra Goebbels, Nicole Schaeren-Wiemers, Klaus-Armin Nave, Hauke B Werner

Abstract read
In one paragraph

Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing 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

43 citing papers in PubMed.

  1. Article
  2. Review
  3. Mechanobiology of Myelin Generation/Regeneration in Health and Disease.Results and problems in cell differentiation · 2026
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Oligodendrocytes: Myelination, Plasticity, and Axonal Support.Cold Spring Harbor perspectives in biology · 2024
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  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

10 authors.

Julia PatzigDepartment of Neurogenetics, Max Planck Institute of Experimental Medicine, Goettingen, Germany.
Michelle S ErwigDepartment of Neurogenetics, Max Planck Institute of Experimental Medicine, Goettingen, Germany.
Stefan TenzerInstitute of Immunology, University Medical Center, Johannes Gutenberg University, Mainz, Germany.
Kathrin KuschDepartment of Neurogenetics, Max Planck Institute of Experimental Medicine, Goettingen, Germany.
Payam DibajDepartment of Neurogenetics, Max Planck Institute of Experimental Medicine, Goettingen, Germany.
Wiebke MöbiusDepartment of Neurogenetics, Max Planck Institute of Experimental Medicine, Goettingen, Germany.
Sandra GoebbelsDepartment of Neurogenetics, Max Planck Institute of Experimental Medicine, Goettingen, Germany.
Nicole Schaeren-WiemersDepartement of Biomedicine, University Hospital Basel, Basel, Switzerland.
Klaus-Armin NaveDepartment of Neurogenetics, Max Planck Institute of Experimental Medicine, Goettingen, Germany.
Hauke B WernerDepartment of Neurogenetics, Max Planck Institute of Experimental Medicine, Goettingen, Germany.ORCID 0000-0002-7710-5738

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myelination of axons facilitates rapid impulse propagation in the nervous system. The axon/myelin-unit becomes impaired in myelin-related disorders and upon normal aging. However, the molecular cause of many pathological features, including the frequently observed myelin outfoldings, remained unknown. Using label-free quantitative proteomics, we find that the presence of myelin outfoldings correlates with a loss of cytoskeletal septins in myelin. Regulated by phosphatidylinositol-(4,5)-bisphosphate (PI(4,5)P2)-levels, myelin septins (SEPT2/SEPT4/SEPT7/SEPT8) and the PI(4,5)P2-adaptor anillin form previously unrecognized filaments that extend longitudinally along myelinated axons. By confocal microscopy and immunogold-electron microscopy, these filaments are localized to the non-compacted adaxonal myelin compartment. Genetic disruption of these filaments in Sept8-mutant mice causes myelin outfoldings as a very specific neuropathology. Septin filaments thus serve an important function in scaffolding the axon/myelin-unit, evidently a late stage of myelin maturation. We propose that pathological or aging-associated diminishment of the septin/anillin-scaffold causes myelin outfoldings that impair the normal nerve conduction velocity.

Indexed as

Neural ConductionAnimalsCentral Nervous SystemContractile ProteinsCytoskeletonGene Knockout TechniquesGene TargetingMiceMicroscopy, ConfocalMicroscopy, ImmunoelectronMyelin SheathNerve Fibers, MyelinatedProtein MultimerizationProteomeProteomicsSeptinsanillinContractile ProteinsProteomeSeptinsglial cellslabel-free proteomicsmousemyelinated axonsmyelin structureneuropathologyneuroscienceseptin cytoskeleton

Identifiers

PMID27504968
PMCPMC4978525

What OpenQuestion holds

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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.