AXONAL GROWTH-RELATED CELL-SURFACE MOLECULE, NEURIN-1, INVOLVED IN NEURON-GLIA INTERACTION

Citation
H. Asou et al., AXONAL GROWTH-RELATED CELL-SURFACE MOLECULE, NEURIN-1, INVOLVED IN NEURON-GLIA INTERACTION, Journal of neuroscience research, 45(5), 1996, pp. 571-587
Citations number
49
Categorie Soggetti
Neurosciences
ISSN journal
03604012
Volume
45
Issue
5
Year of publication
1996
Pages
571 - 587
Database
ISI
SICI code
0360-4012(1996)45:5<571:AGCMNI>2.0.ZU;2-C
Abstract
We purified and characterized a novel axonal growth-related molecule, neurin-1, which is anchored to the surface membrane via a phosphatidyl inositol (PI) linkage, This molecule was detected by a combination of phosphatidylinositol-specific phospholipase C (PI-PLC) treatment from detergent-soluble mouse brain membranes and subsequent Western blot an alysis with monoclonal antibody (MAb 2A), Neurin-1 is immunologically distinct from other known axonal growth associated surface glycoprotei ns, In immunoblots of embryonic mouse brain membrane, the MAb 2A recog nized a single band at approximately 68 kDa, and showed that neurin-1 is mainly associated with fiber-containing regions of developing embry onic mouse brain, Expression is immunohistochemically similar to that of cell adhesion molecule L1, but in comparison, neurin-1 appears some what later. Late in embryonic development, neurin-1 appeared to be mor e stage- and region-specific, Its precise localization at the neural c ell surface membranes was confirmed by immune-electron microscopy usin g labeled and cultured live nerve cells, Neurin-1 was found only on th e surface of the axon and growth cone, Neurin-1, otherwise termed PI a nchor protein, corresponds closely in function to the other PI-anchore d cell adhesion molecules, Anti-neurin-1 antibody (MAb 2A), however, p erturbs the axonal growth and neural cell migration from the astrocyte feeder layer cultures, These results suggest that neurin-1 is one of the important cell surface molecules mediated in the neuron and glial cell interaction. (C) 1996 Wiley-Liss, Inc.