ArticleDevelopment (Cambridge, England)2011
Non-redundant function of dystroglycan and β1 integrins in radial sorting of axons.
Article in Development (Cambridge, England), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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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.
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Who cites it
39 citing papers in PubMed, 67 citations in OpenAlex.
- Myelination and Remyelination in Peripheral Nerve Injury: Mechanisms, Regulation, and Therapeutic Perspectives.MedComm · 2026Review
- Chemogenetic Schwann cell activation impairs early myelination and triggers adult demyelination in the peripheral nervous system.Frontiers in cellular neuroscience · 2026Article
- Mechanobiology of Myelin Generation/Regeneration in Health and Disease.Results and problems in cell differentiation · 2026Review
- The STRIPAK complex is required for radial sorting and laminin receptor expression in Schwann cells.Cell reports · 2025Article
- Pleiotrophin-Neuregulin1 promote axon regeneration and sorting in conduit repair of critical nerve gap injuries.Research square · 2023Article
- Nerve pathology is prevented by linker proteins in mouse models forPNAS nexus · 2023Article
- Review
- Delta/Notch signaling in glia maintains motor nerve barrier function and synaptic transmission by controlling matrix metalloproteinase expression.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Disruption of Endosomal Sorting in Schwann Cells Leads to Defective Myelination and Endosomal Abnormalities Observed in Charcot-Marie-Tooth Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Ninj2 regulates Schwann cells development by interfering laminin-integrin signaling.Theranostics · 2022Article
- Four Seasons for Schwann Cell Biology, Revisiting Key Periods: Development, Homeostasis, Repair, and Aging.Biomolecules · 2021Review
- Peripheral Nerve Development and the Pathogenesis of Peripheral Neuropathy: the Sorting Point.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Review
- αGlia · 2021Article
- Congenital hearing impairment associated with peripheral cochlear nerve dysmyelination in glycosylation-deficient muscular dystrophy.PLoS genetics · 2020Article
- Adult tissue-derived neural crest-like stem cells: Sources, regulatory networks, and translational potential.Stem cells translational medicine · 2020Review
- LAMA2 Neuropathies: Human Findings and Pathomechanisms From Mouse Models.Frontiers in molecular neuroscience · 2020Article
- Laminin α2 controls mouse and human stem cell behaviour during midbrain dopaminergic neuron development.Development (Cambridge, England) · 2019Article
- Ral GTPases in Schwann cells promote radial axonal sorting in the peripheral nervous system.The Journal of cell biology · 2019Article
- Article
- Linker Protein Repair of LAMA2 Dystrophic Neuromuscular Basement Membranes.Frontiers in molecular neuroscience · 2019Review
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Radial sorting allows the segregation of axons by a single Schwann cell (SC) and is a prerequisite for myelination during peripheral nerve development. Radial sorting is impaired in models of human diseases, congenital muscular dystrophy (MDC) 1A, MDC1D and Fukuyama, owing to loss-of-function mutations in the genes coding for laminin α2, Large or fukutin glycosyltransferases, respectively. It is not clear which receptor(s) are activated by laminin 211, or glycosylated by Large and fukutin during sorting. Candidates are αβ1 integrins, because their absence phenocopies laminin and glycosyltransferase deficiency, but the topography of the phenotypes is different and β1 integrins are not substrates for Large and fukutin. By contrast, deletion of the Large and fukutin substrate dystroglycan does not result in radial sorting defects. Here, we show that absence of dystroglycan in a specific genetic background causes sorting defects with topography identical to that of laminin 211 mutants, and recapitulating the MDC1A, MDC1D and Fukuyama phenotypes. By epistasis studies in mice lacking one or both receptors in SCs, we show that only absence of β1 integrins impairs proliferation and survival, and arrests radial sorting at early stages, that β1 integrins and dystroglycan activate different pathways, and that the absence of both molecules is synergistic. Thus, the function of dystroglycan and β1 integrins is not redundant, but is sequential. These data identify dystroglycan as a functional laminin 211 receptor during axonal sorting and the key substrate relevant to the pathogenesis of glycosyltransferase congenital muscular dystrophies.
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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.