MICE DEFICIENT FOR THE MYELIN-ASSOCIATED GLYCOPROTEIN SHOW SUBTLE ABNORMALITIES IN MYELIN

Using homologous recombination in embryonic stem cells, we have genera ted mice with a null mutation in the gene encoding the myelin-associat ed glycoprotein (MAG), a recognition molecule implicated in myelin for mation. MAG-deficient mice appeared normal in motor coordination and s patial learning tasks. Normal myelin structure and nerve conduction in the PNS, with N-CAM overexpression at sites normally expressing MAG, suggested compensatory mechanisms. In the CNS, the onset of myelinatio n was delayed, and subtle morphological abnormalities were detected in that the content of oligodendrocyte cytoplasm at the inner aspect of most myelin sheaths was reduced and that some axons were surrounded by two or more myelin sheaths. These observations suggest that MAG parti cipates in the formation of the periaxonal cytoplasmic collar of oligo dendrocytes and in the recognition between oligodendrocyte processes a nd axons.