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Published 4 February 2002. doi:10.1083/jcb.200111047
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© The Rockefeller University Press, 0021-9525/2002/2/567 $5.00
The Journal of Cell Biology, Volume 156, Number 3, February 4, 2002 567-577

Article

 Myelin-associated glycoprotein and myelin galactolipids stabilize developing axo-glial interactions

Jill Marcus1,2, Jeffrey L. Dupree1,5 and Brian Popko1,2,3,4

1 UNC Neuroscience Center
2 Curriculum in Neurobiology
3 Department of Biochemistry and Biophysics
4 Program in Molecular Biology and Biotechnology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599
5 Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599

Address correspondence to Dr. Brian Popko, The Jack Miller Center for Peripheral Neuropathy, The University of Chicago, 5841 S. Maryland Ave., MC2030, Chicago, IL 60637-1470. Tel.: (773) 702-4953. Fax: (773) 702-9076. E-mail: bpopko{at}neurology.bsd.uchicago.edu

We have analyzed mice that lack both the myelin-associated glycoprotein (MAG) and the myelin galactolipids, two glial components implicated in mediating axo-glial interactions during the myelination process. The single-mutant mice produce abnormal myelin containing similar ultrastructural abnormalities, suggesting that these molecules may play an overlapping role in myelin formation. Furthermore, the absence of the galactolipids results in a disruption in paranodal axo-glial interactions, and we show here that similar, albeit less severe, abnormalities exist in the developing MAG mutant. In the double-mutant mice, maintenance of axo-glial adhesion is significantly more affected than in the single mutants, supporting the overlapping function hypothesis. We also show that independently of MAG, galactolipids, and paranodal junctional components, immature nodes of Ranvier form normally, but rapidly destabilize in their absence. These data indicate that distinct molecular mechanisms are responsible for the formation and maintenance of axo-glial interactions.

Key Words: myelination; MAG; galactolipids; periaxon; nodes


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