Document Detail

Overexpression of Fyn tyrosine kinase causes abnormal development of primary sensory neurons in Xenopus laevis embryos.
MedLine Citation:
PMID:  11422288     Owner:  NLM     Status:  MEDLINE    
The expression and function of the Src family protein tyrosine kinase Fyn in Xenopus laevis embryos have been examined. In situ hybridization analysis demonstrated nervous system-specific expression of Fyn mRNA in tail-bud embryos. However, a class of primary sensory neurons; that is, Rohon-Beard (RB) neurons, which is positive for immunoglobulin superfamily cell adhesion molecules (CAM), neural cell adhesion molecule (N-CAM) and contactin, is devoid of Fyn expression. Injection of Fyn mRNA into one of the blastomeres at the 2-cell stage led to overexpression of Fyn in the injected half of the tail-bud embryos. Immunolabeling of the embryos with anti-HNK-1 antibody revealed that the peripheral axons of RB neurons were partially misguided and bound to each other to form abnormal subcutaneous fascicles. Similar abnormality was induced by injection of the Fyn overexpression vector. The incidence of abnormality appeared dose-dependent, being 68-92% of the injected embryos at 50-400 pg of mRNA. Co-injection of the contactin antisense vector depleted contactin mRNA accumulation without affecting Fyn overexpression and reduced the incidence of the abnormal RB-cell phenotype. However, the N-CAM antisense was ineffective in reducing this abnormality. These results suggest that Fyn can modify signals regulating axonal guidance or fasciculation in the developing X. laevis nervous system and that contactin may affect this action of Fyn.
R Saito; N Fujita; S Nagata
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Development, growth & differentiation     Volume:  43     ISSN:  0012-1592     ISO Abbreviation:  Dev. Growth Differ.     Publication Date:  2001 Jun 
Date Detail:
Created Date:  2001-06-25     Completed Date:  2001-11-01     Revised Date:  2012-06-05    
Medline Journal Info:
Nlm Unique ID:  0356504     Medline TA:  Dev Growth Differ     Country:  Japan    
Other Details:
Languages:  eng     Pagination:  229-38     Citation Subset:  IM    
Department of Chemical and Biological Sciences, Faculty of Science, Japan Women's University, Tokyo 112-8681, Japan.
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MeSH Terms
Cell Adhesion Molecules, Neuronal / genetics,  metabolism
Central Nervous System / embryology*
Embryo, Nonmammalian / physiology*
Gene Expression
In Situ Hybridization
Neurons, Afferent / cytology,  physiology*
Proto-Oncogene Proteins / genetics,  metabolism*
Proto-Oncogene Proteins c-fyn
RNA, Antisense / genetics,  metabolism
Xenopus Proteins
Xenopus laevis
Reg. No./Substance:
0/Cell Adhesion Molecules, Neuronal; 0/Proto-Oncogene Proteins; 0/RNA, Antisense; 0/Xenopus Proteins; EC protein, Xenopus; EC Proteins c-fyn

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