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Titolo:
A unique role for fyn in CNS myelination
Autore:
Sperber, BR; Boyle-Walsh, EA; Engleka, MJ; Gadue, P; Peterson, AC; Stein, PL; Scherer, SS; McMorris, FA;
Indirizzi:
Wistar Inst, Philadelphia, PA 19104 USA Wistar Inst Philadelphia PA USA 19104 ar Inst, Philadelphia, PA 19104 USA Univ Penn, Grad Grp Neurosci, Philadelphia, PA 19104 USA Univ Penn Philadelphia PA USA 19104 Neurosci, Philadelphia, PA 19104 USA Univ Penn, Dept Neurol, Philadelphia, PA 19104 USA Univ Penn PhiladelphiaPA USA 19104 pt Neurol, Philadelphia, PA 19104 USA McGill Univ, Royal Victoria Hosp, Dept Neurol & Neurosurg, Montreal, PQ H3A 1A1, Canada McGill Univ Montreal PQ Canada H3A 1A1 surg, Montreal, PQ H3A 1A1, Canada
Titolo Testata:
JOURNAL OF NEUROSCIENCE
fascicolo: 6, volume: 21, anno: 2001,
pagine: 2039 - 2047
SICI:
0270-6474(20010315)21:6<2039:AURFFI>2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
TYROSINE KINASE; MUTANT MICE; SEVERE HYPOMYELINATION; DOWN-REGULATION; DEFICIENT MICE; RAT-BRAIN; OLIGODENDROCYTES; SRC; ACTIVATION; ANTIGEN;
Keywords:
myelin; oligodendrocyte; corpus callosum; spinal cord; tyrosine kinase; Fyn; Src; Lyn; Yes; development; knock-out;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
39
Recensione:
Indirizzi per estratti:
Indirizzo: McMorris, FA Wistar Inst, Philadelphia, PA 19104 USA Wistar Inst Philadelphia PA USA 19104 adelphia, PA 19104 USA
Citazione:
B.R. Sperber et al., "A unique role for fyn in CNS myelination", J NEUROSC, 21(6), 2001, pp. 2039-2047

Abstract

We analyzed the role of Fyn tyrosine kinase in CNS myelination by using fyn(-/-) null mutant mice, which express no Fyn protein. We found a severe myelin deficit in forebrain at all ages from 14 d to 1 year. The deficit was maximal at 1 month of age and was similar regardless of mouse strain background or whether it was determined by bulk isolation of myelin or by quantitation of myelin basic protein. To determine the cellular basis of the myelin deficit, we counted oligodendrocytes in tissue sections of mice expressing oligodendrocyte-targeted beta -galactosidase, and we used light and electron microscopy to examine the number and morphology of myelinated fibers and size of myelinated CNS structures. All of these parameters were reduced in fyn(-/-) mice. Unexpectedly, there were regional differences in the myelin deficit; in contrast to forebrain, fyn(-/-) cervical spinal cord exhibited no reduction in myelin content, number of oligodendrocytes, or number of myelinated fibers, nor was myelination delayed developmentally. We found that oligodendrocytes express Src, but there was no significant reduction of myelin content in null mutants lacking the Fyn-related kinases Src, Yes, orLyn. Finally, we investigated the molecular features of Fyn that are required for myelination and found that a single amino acid substitution, which abolishes the tyrosine kinase activity of Fyn, resulted in a myelin deficitas great as that observed in the complete absence of Fyn protein. These results demonstrate that Fyn plays a unique role in myelination, one that requires its kinase activity.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/11/20 alle ore 15:11:09