Evidence map›Paper›PMID 27855200›Full record

ArticlePloS one2016

Mammalian-Specific Central Myelin Protein Opalin Is Redundant for Normal Myelination: Structural and Behavioral Assessments.

Fumio Yoshikawa, Yumi Sato, Koujiro Tohyama, Takumi Akagi, Tamio Furuse, Tetsushi Sadakata, Mika Tanaka, Yo Shinoda, Tsutomu Hashikawa, Shigeyoshi Itohara and 4 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.0field-weighted citation impact, top 21% 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

10 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Repeated ablations of mature Tmem10Cell death & disease · 2025
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  5. Zinc-Finger Protein ZFP488 Regulates the Timing of Oligodendrocyte Myelination and Remyelination.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  6. OPALIN is an LGI1 receptor promoting oligodendrocyte differentiation.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  7. Article
  8. MKK7 deficiency in mature neurons impairs parental behavior in mice.Genes to cells : devoted to molecular & cellular mechanisms · 2021
    Article
  9. Article
  10. 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

14 authors at 7 institutions in 3 countries.

Fumio YoshikawaLaboratory for Molecular Neurogenesis, RIKEN Brain Science Institute, Wako, Saitama, 351-0198, Japan.
Yumi SatoLaboratory for Molecular Neurogenesis, RIKEN Brain Science Institute, Wako, Saitama, 351-0198, Japan.
Koujiro TohyamaThe Center for Electron Microscopy and Bio-Imaging Research and Department of Physiology, Iwate Medical University, Morioka, Iwate, 020-8505, Japan.
Takumi AkagiSupport Unit for Neuromorphological Analysis, RIKEN Brain Science Institute, Wako, Saitama, 351-0198, Japan.
Tamio FuruseTechnology and Development Team for Mouse Phenotype Analysis, RIKEN BioResource Center, Tsukuba, Ibaraki, 305-0074, Japan.
Tetsushi SadakataLaboratory for Molecular Neurogenesis, RIKEN Brain Science Institute, Wako, Saitama, 351-0198, Japan.
Mika TanakaLaboratory for Behavioral Genetics, RIKEN Brain Science Institute, Wako, Saitama, 351-0198, Japan.
Yo ShinodaLaboratory for Molecular Neurogenesis, RIKEN Brain Science Institute, Wako, Saitama, 351-0198, Japan.
Tsutomu HashikawaSupport Unit for Neuromorphological Analysis, RIKEN Brain Science Institute, Wako, Saitama, 351-0198, Japan.
Shigeyoshi ItoharaLaboratory for Behavioral Genetics, RIKEN Brain Science Institute, Wako, Saitama, 351-0198, Japan.
Yoshitake SanoDepartment of Applied Biological Science, Faculty of Science and Technology, Tokyo University of Science, Chiba, 278-8510, Japan.
M Said GhandourUnite´ Mixte de Recherche 7357, Université de Strasbourg, Strasbourg, 67085, France and Department of Anatomy and Neurobiology, Virginia Commonwealth University, Richmond, Virginia, United States of America.
Shigeharu WakanaTechnology and Development Team for Mouse Phenotype Analysis, RIKEN BioResource Center, Tsukuba, Ibaraki, 305-0074, Japan.
Teiichi FuruichiLaboratory for Molecular Neurogenesis, RIKEN Brain Science Institute, Wako, Saitama, 351-0198, Japan.ORCID http://orcid.org/0000-0002-9676-1888
RIKEN Center for Brain Science · JPRIKEN BioResource Research Center · JPTokyo University of Science · JPGunma University · JPIwate Medical University · JPTokyo University of Pharmacy and Life Sciences · JPVirginia Commonwealth University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Opalin, a central nervous system-specific myelin protein phylogenetically unique to mammals, has been suggested to play a role in mammalian-specific myelin. To elucidate the role of Opalin in mammalian myelin, we disrupted the Opalin gene in mice and analyzed the impacts on myelination and behavior. Opalin-knockout (Opalin-/-) mice were born at a Mendelian ratio and had a normal body shape and weight. Interestingly, Opalin-/- mice had no obvious abnormalities in major myelin protein compositions, expression of oligodendrocyte lineage markers, or domain organization of myelinated axons compared with WT mice (Opalin+/+) mice. Electron microscopic observation of the optic nerves did not reveal obvious differences between Opalin+/+ and Opalin-/- mice in terms of fine structures of paranodal loops, transverse bands, and multi-lamellae of myelinated axons. Moreover, sensory reflex, circadian rhythm, and locomotor activity in the home cage, as well as depression-like behavior, in the Opalin-/- mice were indistinguishable from the Opalin+/+ mice. Nevertheless, a subtle but significant impact on exploratory activity became apparent in Opalin-/- mice exposed to a novel environment. These results suggest that Opalin is not critical for central nervous system myelination or basic sensory and motor activities under conventional breeding conditions, although it might be required for fine-tuning of exploratory behavior.

Indexed as

Behavior, AnimalAnimalsAstrocytesAxonsBody WeightBrainCell CommunicationCell DifferentiationExploratory BehaviorImmunoblottingMammalsMice, Inbred C57BLMice, Inbred ICRMice, KnockoutMyelin ProteinsMyelin SheathMyelin ProteinsOpalin protein, mouse

Identifiers

PMID27855200
PMCPMC5113975
OpenAlexW2555975786

What OpenQuestion holds

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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.