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Paranodal axoglial junctions are critical for maintaining the segregation of axonal domains along myelinated axons; however, the proteins required to organize and maintain this structure are not fully understood. Netrin-1 and its receptor Deleted in Colorectal Cancer (DCC) are proteins enriched at paranodes that are expressed by neurons and oligodendrocytes. To identify the specific function of DCC expressed by oligodendrocytes in vivo, we selectively eliminated DCC from mature myelinating oligodendrocytes using an inducible cre regulated by the proteolipid protein promoter. We demonstrate that DCC deletion results in progressive disruption of the organization of axonal domains, myelin ultrastructure, and myelin protein composition. Conditional DCC knock-out mice develop balance and coordination deficits and exhibit decreased conduction velocity. We conclude that DCC expression by oligodendrocytes is required for the maintenance and stability of myelin in vivo, which is essential for proper signal conduction in the CNS.

Titel:	Progressive disorganization of paranodal junctions and compact myelin due to loss of DCC expression by oligodendrocytes.
Autor/in / Beteiligte Person:	Bull, SJ ; Bin, JM ; Beaumont, E ; Boutet, A ; Krimpenfort, P ; Sadikot, AF ; Kennedy, TE
Link:	Full Text Finder (Volltext)
Zeitschrift:	The Journal of neuroscience : the official journal of the Society for Neuroscience, Jg. 34 (2014-07-16), Heft 29, S. 9768-78
Veröffentlichung:	Washington, DC : Society for Neuroscience ; <i>Original Publication</i>: [Baltimore, Md.] : The Society, c1981-, 2014
Medientyp:	academicJournal
ISSN:	1529-2401 (electronic)
DOI:	10.1523/JNEUROSCI.0448-14.2014
Schlagwort:	Animals Axons physiology Cell Count DCC Receptor Embryo, Mammalian Estrogen Antagonists pharmacology Exploratory Behavior physiology Gap Junctions ultrastructure Integrases genetics Mice Mice, Transgenic Microscopy, Electron, Transmission Myelin Proteolipid Protein genetics Myelin Proteolipid Protein metabolism Myelin Sheath ultrastructure Neural Conduction drug effects Neural Conduction genetics Oligodendroglia ultrastructure Psychomotor Disorders genetics Ranvier's Nodes metabolism Ranvier's Nodes ultrastructure Receptors, Cell Surface genetics Tamoxifen pharmacology Tumor Suppressor Proteins genetics Gap Junctions physiology Gene Expression Regulation, Developmental drug effects Gene Expression Regulation, Developmental genetics Myelin Sheath physiology Oligodendroglia metabolism Receptors, Cell Surface deficiency Tumor Suppressor Proteins deficiency
Sonstiges:	Nachgewiesen in: MEDLINE Sprachen: English Publication Type: Journal Article; Research Support, Non-U.S. Gov't Language: English [J Neurosci] 2014 Jul 16; Vol. 34 (29), pp. 9768-78. MeSH Terms: Gene Expression Regulation, Developmental* / drug effects ; Gene Expression Regulation, Developmental* / genetics ; Gap Junctions / physiology ; Myelin Sheath / physiology ; Oligodendroglia / metabolism ; Receptors, Cell Surface / deficiency ; Tumor Suppressor Proteins / *deficiency ; Animals ; Axons / physiology ; Cell Count ; DCC Receptor ; Embryo, Mammalian ; Estrogen Antagonists / pharmacology ; Exploratory Behavior / physiology ; Gap Junctions / ultrastructure ; Integrases / genetics ; Mice ; Mice, Transgenic ; Microscopy, Electron, Transmission ; Myelin Proteolipid Protein / genetics ; Myelin Proteolipid Protein / metabolism ; Myelin Sheath / ultrastructure ; Neural Conduction / drug effects ; Neural Conduction / genetics ; Oligodendroglia / ultrastructure ; Psychomotor Disorders / genetics ; Ranvier's Nodes / metabolism ; Ranvier's Nodes / ultrastructure ; Receptors, Cell Surface / genetics ; Tamoxifen / pharmacology ; Tumor Suppressor Proteins / genetics References: Cell. 1996 Jul 26;86(2):209-19. 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(PMID: 9464989) ; J Neurosci Res. 2004 Sep 1;77(5):690-700. (PMID: 15352215) Grant Information: Canada Canadian Institutes of Health Research Contributed Indexing: Keywords: DCC; caspr; myelin; netrin; oligodendrocyte; paranode Substance Nomenclature: 0 (DCC Receptor) ; 0 (Dcc protein, mouse) ; 0 (Estrogen Antagonists) ; 0 (Myelin Proteolipid Protein) ; 0 (Plp1 protein, mouse) ; 0 (Receptors, Cell Surface) ; 0 (Tumor Suppressor Proteins) ; 094ZI81Y45 (Tamoxifen) ; EC 2.7.7.- (Cre recombinase) ; EC 2.7.7.- (Integrases) Entry Date(s): Date Created: 20140718 Date Completed: 20140905 Latest Revision: 20211021 Update Code: 20231215 PubMed Central ID: PMC6608320

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Progressive disorganization of paranodal junctions and compact myelin due to loss of DCC expression by oligodendrocytes.