ArticleThe Journal of biological chemistry2015
Microprocessor complex subunit DiGeorge syndrome critical region gene 8 (Dgcr8) is required for schwann cell myelination and myelin maintenance.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
- DGCR8 microprocessor defect characterizes familial multinodular goiter with schwannomatosis.The Journal of clinical investigation · 2020Trial
- Enhancer-driven Shh signaling promotes glia-to-mesenchyme transition during bone repair.Bone research · 2025Article
- Development of a ZRS Reporter System for the Newt (Biomedicines · 2024Article
- Schwann Cell Development and Myelination.Cold Spring Harbor perspectives in biology · 2024Review
- JUN Regulation of Injury-Induced Enhancers in Schwann Cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Lessons from Injury: How Nerve Injury Studies Reveal Basic Biological Mechanisms and Therapeutic Opportunities for Peripheral Nerve Diseases.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Review
- Review
- Article
- Hedging against Neuropathic Pain: Role of Hedgehog Signaling in Pathological Nerve Healing.International journal of molecular sciences · 2020Review
- ADAR1 mediated regulation of neural crest derived melanocytes and Schwann cell development.Nature communications · 2020Article
- Novel Glial Cell Functions: Extensive Potency, Stem Cell-Like Properties, and Participation in Regeneration and Transdifferentiation.Frontiers in cell and developmental biology · 2020Review
- In the line-up: deleted genes associated with DiGeorge/22q11.2 deletion syndrome: are they all suspects?Journal of neurodevelopmental disorders · 2019Review
- Dgcr8 knockout approaches to understand microRNA functions in vitro and in vivo.Cellular and molecular life sciences : CMLS · 2019Review
- The Success and Failure of the Schwann Cell Response to Nerve Injury.Frontiers in cellular neuroscience · 2019Review
- Article
- Polycomb repression regulates Schwann cell proliferation and axon regeneration after nerve injury.Glia · 2018Article
- Egr2-dependent microRNA-138 is dispensable for peripheral nerve myelination.Scientific reports · 2018Article
- A DGCR8-Independent Stable MicroRNA Expression Strategy Reveals Important Functions of miR-290 and miR-183-182 Families in Mouse Embryonic Stem Cells.Stem cell reports · 2017Article
- Comparison of DNA Methylation in Schwann Cells before and after Peripheral Nerve Injury in Rats.BioMed research international · 2017Article
- Epigenomic reprogramming in peripheral nerve injury.Neural regeneration research · 2016Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
We investigated the role of a key component of the Microprocessor complex, DGCR8, in the regulation of myelin formation and maintenance. We found that conditionally ablating Dgcr8 in Schwann cells (SCs) during development results in an arrest of SC differentiation. Dgcr8 conditional knock-out (cKO) SCs fail to form 1:1 relationships with axons or, having achieved this, fail to form myelin sheaths. The expression of genes normally found in immature SCs, such as sex-determining region Y-box 2 (Sox2), is increased in Dgcr8 cKO SCs, whereas the expression of myelin-related genes, including the master regulatory transcription factor early growth response 2 (Egr2), is decreased. Additionally, expression of a novel gene expression program involving sonic hedgehog (Shh), activated de novo in injured nerves, is elevated in Dgcr8 cKOs but not in Egr2 null mice, a model of SC differentiation arrest, suggesting that the injury-related gene expression program in Dgcr8 cKOs cannot be attributed to differentiation arrest. Inducible ablation of Dgcr8 in adult SCs results in gene expression changes similar to those found in cKOs, including an increase in the expression of Sox2 and Shh. Analyses of these nerves mainly reveal normal myelin thickness and axon size distribution but some dedifferentiated SCs and increased macrophage infiltration. Together our data suggest that Dgcr8 is responsible for modulation of gene expression programs underlying myelin formation and maintenance as well as suppression of an injury-related gene expression program.
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Registered trials
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