ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009
A laminin-2, dystroglycan, utrophin axis is required for compartmentalization and elongation of myelin segments.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 69 citations in OpenAlex.
- The STRIPAK complex is required for radial sorting and laminin receptor expression in Schwann cells.Cell reports · 2025Article
- Schwann Cell Development and Myelination.Cold Spring Harbor perspectives in biology · 2024Review
- Upregulation of large myelin protein zero leads to Charcot-Marie-Tooth disease-like neuropathy in mice.Communications biology · 2020Article
- Flexible Players within the Sheaths: The Intrinsically Disordered Proteins of Myelin in Health and Disease.Cells · 2020Review
- Novel mutation in the periaxin gene causal to Charcot-Marie-Tooth disease type 4F.The Journal of international medical research · 2020Article
- Brain Dysfunction in LAMA2-Related Congenital Muscular Dystrophy: Lessons From Human Case Reports and Mouse Models.Frontiers in molecular neuroscience · 2020Article
- LAMA2 Neuropathies: Human Findings and Pathomechanisms From Mouse Models.Frontiers in molecular neuroscience · 2020Article
- Proximity biotinylation identifies a set of conformation-specific interactions between Merlin and cell junction proteins.Science signaling · 2019Article
- GPR56/ADGRG1 regulates development and maintenance of peripheral myelin.The Journal of experimental medicine · 2018Article
- Differential effects of myostatin deficiency on motor and sensory axons.Muscle & nerve · 2017Article
- Laminin 211 inhibits protein kinase A in Schwann cells to modulate neuregulin 1 type III-driven myelination.PLoS biology · 2017Article
- Myelinating Schwann Cell Polarity and Mechanically-Driven Myelin Sheath Elongation.Frontiers in cellular neuroscience · 2017Review
- Zeb2: Inhibiting the inhibitors in Schwann cells.Neurogenesis (Austin, Tex.) · 2017Article
- Optimal myelin elongation relies on YAP activation by axonal growth and inhibition by Crb3/Hippo pathway.Nature communications · 2016Article
- How Schwann Cells Sort Axons: New Concepts.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2016Review
- Dynamic regulation of Schwann cell enhancers after peripheral nerve injury.The Journal of biological chemistry · 2015Article
- Perlecan is recruited by dystroglycan to nodes of Ranvier and binds the clustering molecule gliomedin.The Journal of cell biology · 2015Article
- Autophagy is involved in the reduction of myelinating Schwann cell cytoplasm during myelin maturation of the peripheral nerve.PloS one · 2015Article
- Schwann Cell Expressed Nogo-B Modulates Axonal Branching of Adult Sensory Neurons Through the Nogo-B Receptor NgBR.Frontiers in cellular neuroscience · 2015Article
- Calcium release from intra-axonal endoplasmic reticulum leads to axon degeneration through mitochondrial dysfunction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
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Authors and funding
7 authors at 6 institutions in 3 countries.
Funding
Abstract
Animal and plant cells compartmentalize to perform morphogenetic functions. Compartmentalization of myelin-forming Schwann cells may favor elongation of myelin segments to the size required for efficient conduction of nerve impulses. Compartments in myelinated fibers were described by Ramón y Cajal and depend on periaxin, mutated in the hereditary neuropathy Charcot-Marie-Tooth disease type 4F (Charcot-Marie-Tooth 4F). Lack of periaxin in mice causes loss of compartments, formation of short myelin segments (internodes) and reduced nerve conduction velocity. How compartments are formed and maintained, and their relevance to human neuropathies is largely unknown. Here we show that formation of compartments around myelin is driven by the actin cytoskeleton, and maintained by actin and tubulin fences through linkage to the dystroglycan complex. Compartmentalization and establishment of correct internodal length requires the presence of glycosylated dystroglycan, utrophin and extracellular laminin-2/211. A neuropathic patient with reduced internodal length and nerve conduction velocity because of absence of laminin-2/211 (congenital muscular dystrophy 1A) also shows abnormal compartmentalization. These data link formation of compartments through a laminin2, dystroglycan, utrophin, actin axis to internodal length, and provide a common pathogenetic mechanism for two inherited human neuropathies. Other cell types may exploit dystroglycan complexes in similar fashions to create barriers and compartments.
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