Talk:Neural Crest - Schwann Cell Development
|About Discussion Pages|
Cite this page: Hill, M.A. (2019, October 22) Embryology Neural Crest - Schwann Cell Development. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Neural_Crest_-_Schwann_Cell_Development
Dual origin of enteric neurons in vagal Schwann cell precursors and the sympathetic neural crest
Proc Natl Acad Sci U S A. 2017 Nov 7;114(45):11980-11985. doi: 10.1073/pnas.1710308114. Epub 2017 Oct 24.
Espinosa-Medina I1, Jevans B2, Boismoreau F1, Chettouh Z1, Enomoto H3, Müller T4, Birchmeier C4, Burns AJ2,5, Brunet JF6.
Most of the enteric nervous system derives from the "vagal" neural crest, lying at the level of somites 1-7, which invades the digestive tract rostro-caudally from the foregut to the hindgut. Little is known about the initial phase of this colonization, which brings enteric precursors into the foregut. Here we show that the "vagal crest" subsumes two populations of enteric precursors with contrasted origins, initial modes of migration, and destinations. Crest cells adjacent to somites 1 and 2 produce Schwann cell precursors that colonize the vagus nerve, which in turn guides them into the esophagus and stomach. Crest cells adjacent to somites 3-7 belong to the crest streams contributing to sympathetic chains: they migrate ventrally, seed the sympathetic chains, and colonize the entire digestive tract thence. Accordingly, enteric ganglia, like sympathetic ones, are atrophic when deprived of signaling through the tyrosine kinase receptor ErbB3, while half of the esophageal ganglia require, like parasympathetic ones, the nerve-associated form of the ErbB3 ligand, Neuregulin-1. These dependencies might bear relevance to Hirschsprung disease, with which alleles of Neuregulin-1 are associated. KEYWORDS: Neuregulin1; chicken; enteric nervous system; mouse; neural crest PMID: 29078343 PMCID: PMC5692562 [Available on 2018-05-07] DOI: 10.1073/pnas.1710308114
How Schwann Cells Sort Axons: New Concepts
Neuroscientist. 2016 Jun;22(3):252-65. doi: 10.1177/1073858415572361. Epub 2015 Feb 16.
Feltri ML1, Poitelon Y2, Previtali SC3.
Peripheral nerves contain large myelinated and small unmyelinated (Remak) fibers that perform different functions. The choice to myelinate or not is dictated to Schwann cells by the axon itself, based on the amount of neuregulin I-type III exposed on its membrane. Peripheral axons are more important in determining the final myelination fate than central axons, and the implications for this difference in Schwann cells and oligodendrocytes are discussed. Interestingly, this choice is reversible during pathology, accounting for the remarkable plasticity of Schwann cells, and contributing to the regenerative potential of the peripheral nervous system. Radial sorting is the process by which Schwann cells choose larger axons to myelinate during development. This crucial morphogenetic step is a prerequisite for myelination and for differentiation of Remak fibers, and is arrested in human diseases due to mutations in genes coding for extracellular matrix and linkage molecules. In this review we will summarize progresses made in the last years by a flurry of reverse genetic experiments in mice and fish. This work revealed novel molecules that control radial sorting, and contributed unexpected ideas to our understanding of the cellular and molecular mechanisms that control radial sorting of axons. © The Author(s) 2015. KEYWORDS: Schwann cells; development; human peripheral neuropathies; myelin; peripheral nervous system
Glial versus melanocyte cell fate choice: Schwann cell precursors as a cellular origin of melanocytes
Cell Mol Life Sci. 2010 Sep;67(18):3037-55. Epub 2010 May 9.
Adameyko I, Lallemend F.
Unit of Molecular Neurobiology, Department of Medical Biochemistry and Biophysics, Karolinska Institute, Scheeles väg 1-A1-plan2, 171 77, Stockholm, Sweden. firstname.lastname@example.org Abstract Melanocytes and Schwann cells are derived from the multipotent population of neural crest cells. Although both cell types were thought to be generated through completely distinct pathways and molecular processes, a recent study has revealed that these different cell types are intimately interconnected far beyond previously postulated limits in that they share a common post-neural crest progenitor, i.e. the Schwann cell precursor. This finding raises interesting questions about the lineage relationships of hitherto unrelated cell types such as melanocytes and Schwann cells, and may provide clinical insights into mechanisms of pigmentation disorders and for cancer involving Schwann cells and melanocytes.
Sox10 is required for Schwann cell identity and progression beyond the immature Schwann cell stage
J Cell Biol. 2010 May 17;189(4):701-12. Epub 2010 May 10.
Finzsch M, Schreiner S, Kichko T, Reeh P, Tamm ER, Bösl MR, Meijer D, Wegner M.
Institut für Biochemie, Emil-Fischer-Zentrum, Universität Erlangen-Nürnberg, 91054 Erlangen, Germany.
Abstract Mutations in the transcription factor SOX10 cause neurocristopathies, including Waardenburg-Hirschsprung syndrome and peripheral neuropathies in humans. This is partly attributed to a requirement for Sox10 in early neural crest for survival, maintenance of pluripotency, and specification to several cell lineages, including peripheral glia. As a consequence, peripheral glia are absent in Sox10-deficient mice. Intriguingly, Sox10 continues to be expressed in these cells after specification. To analyze glial functions after specification, we specifically deleted Sox10 in immature Schwann cells by conditional mutagenesis. Mutant mice died from peripheral neuropathy before the seventh postnatal week. Nerve alterations included a thinned perineurial sheath, increased lipid and collagen deposition, and a dramatically altered cellular composition. Nerve conduction was also grossly aberrant, and neither myelinating nor nonmyelinating Schwann cells formed. Instead, axons of different sizes remained unsorted in large bundles. Schwann cells failed to develop beyond the immature stage and were unable to maintain identity. Thus, our study identifies a novel cause for peripheral neuropathies in patients with SOX10 mutations.
PMID: 20457761 http://www.ncbi.nlm.nih.gov/pubmed/20457761
Gliogenesis: historical perspectives, 1839-1985
Adv Anat Embryol Cell Biol. 2009;202:1-109.
Webster H, Aström KE.
Neuroimmunology Branch, National Institute of Neurological Diseases and Stroke MSC, Bethesda, MD 20892-1400, USA. email@example.com
Abstract This historical review of gliogenesis begins with Schwann's introduction of the cell doctrine in 1839. Subsequent microscopic studies revealed the cellular structure of many organs and tissues, but the CNS was thought to be different. In 1864, Virchow created the concept that nerve cells are held together by a "Nervenkitte" which he called"glia" (for glue). He and his contemporaries thought that "glia" was an unstructured, connective tissue-like ground substance that separated nerve cells from each other and from blood vessels. Dieters, a pupil of Virchow, discovered that this ground substance contained cells, which he described and illustrated. Improvements in microscopes and discovery of metallic impregnation methods finally showed convincingly that the "glia" was not a binding substance. Instead, it was composed of cells, each separate and distinct from neighboring cells and each with its own characteristic array of processes. Light microscopic studies of developing and mature nervous tissue led to the discovery of different types of glial cells-astroglia, oligodendroglia, microglia, and ependymal cells in the CNS, and Schwann cells in the peripheral nervous system (PNS). Subsequent studies characterized the origins and development of each type of glial cell. A new era began with the introduction of electron microscopy, immunostaining, and in vitro maintenance of both central and peripheral nervous tissue. Other methods and models greatly expanded our understanding of how glia multiply, migrate, and differentiate. In 1985, almost a century and a half of study had produced substantial progress in our understanding of glial cells, including their origins and development. Major advances were associated with the discovery of new methods. These are summarized first. Then the origins and development of astroglia, oligodendroglia, microglia, ependymal cells, and Schwann cells are described and discussed. In general, morphology is emphasized. Findings related to cytodifferentiation, cellular interactions, functions, and regulation of developing glia have also been included.
PMID: 19230601 http://www.ncbi.nlm.nih.gov/pubmed/19230601