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Myelin associated glycoprotein modulates glia-axon contact in vivo
1Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Canada. chumei.li@utoronto.ca
Abstract:
Myelin-associated glycoprotein (MAG) was postulated to play an important role in myelination. However, we showed previously that MAG null mutants exhibited no gross abnormality in myelination. Ultrastructural studies revealed subtle alterations in periaxonal organisation, indicating a restricted structural role for MAG in the formation and maintenance of periaxonal structures (Li et al., 1994). Here we show that myelination in MAG deficient mice is not as finely controlled as it is in wild type mice. The abnormalities manifest themselves as a decrease in the proportion of myelinated axons and a reciprocal increase in the proportion of unmyelinated axons in mutants' optic nerves. In addition, dysregulated myelination is occasionally observed in the form of multiply myelinated fibres, grouping of myelinated axons and myelin debris by a large myelin sheath, redundant myelin loops and, very rarely, massive myelin surrounding relatively small axons. Thus, in the absence of MAG, some glial cells seem unable to determine when, where and how much myelin should be laid down. These data support the notion of MAG being a glial recognition/adhesion molecule. A model is proposed regarding the roles MAG could play in the formation and maintenance of myelin structure.
Insights
Myelin-associated glycoprotein (MAG) deficiency in mice leads to dysregulated myelination, impacting glial cell control over myelin formation and maintenance. This study reveals subtle but significant abnormalities in MAG-deficient optic nerves.
Area of Science:
- Neuroscience
- Cell Biology
- Developmental Biology
Background:
- Myelin-associated glycoprotein (MAG) was hypothesized to be crucial for myelination.
- Previous studies showed MAG null mutants lacked gross myelination abnormalities but had subtle periaxonal organization defects.
Purpose of the Study:
- To investigate the role of MAG in the fine control of myelination.
- To characterize the myelination defects in MAG-deficient mice.
Main Methods:
- Analysis of MAG null mutant mice.
- Ultrastructural examination of optic nerves.
- Quantitative assessment of myelinated and unmyelinated axons.
Main Results:
- MAG deficiency results in less controlled myelination in mice optic nerves.
- Observed decrease in myelinated axons and increase in unmyelinated axons.
- Dysregulated myelination includes multiply myelinated fibers, myelin debris, and redundant myelin loops.
Conclusions:
- MAG is essential for the precise regulation of myelin sheath formation and maintenance.
- Absence of MAG impairs glial cell ability to control myelination extent and location.
- MAG functions as a glial recognition/adhesion molecule in myelination.