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Myelin basic protein is necessary for the regulation of myelin-associated glycoprotein expression in mouse
J Nakahara1, K Tan-Takeuchi, C Seiwa
1Department of Neurobiology, Tokyo Metropolitan Institute of Gerontology, 35-2 Sakaecho, Itabashi-ku, 173-0015, Tokyo, Japan.
Abstract:
Myelin-associated glycoprotein (MAG) has currently been proposed to be a possible igniter of myelination in the central nervous system. We propose here that myelin basic protein (MBP) is prerequisite, which is more diffusely expressed than MAG in early stages of myelination. MBP-deficient mice show significant reduction of MAG-positive immature oligodendroglia at early stages of myelination, although significant increase of such cells is noted in the adult. MBP/Fyn-double deficient adult mice also show moderate increase of the same type of immature glia, but to a lesser degree than MBP-deficiency alone. The present study suggests that MBP is required for the regulation of MAG expression in oligodendroglia, involving Fyn therein. We discuss the possibility that hitherto unknown molecule, not MAG, may be in responsible for the ignition of the myelination.
Insights
Myelin basic protein (MBP) is crucial for initiating myelination, regulating myelin-associated glycoprotein (MAG) expression in the central nervous system. MBP deficiency impacts immature oligodendroglia development, suggesting a novel ignition molecule for myelination.
Area of Science:
- Neuroscience
- Cell Biology
- Developmental Biology
Background:
- Myelin-associated glycoprotein (MAG) is a proposed initiator of central nervous system myelination.
- The role of myelin basic protein (MBP) in early myelination stages is less understood.
- Oligodendroglia are glial cells responsible for myelin production in the CNS.
Purpose of the Study:
- To investigate the role of myelin basic protein (MBP) in the early stages of central nervous system myelination.
- To determine if MBP is a prerequisite for myelin-associated glycoprotein (MAG) expression.
- To explore the involvement of Fyn kinase in MBP-mediated regulation of MAG.
Main Methods:
- Utilized MBP-deficient mice and MBP/Fyn-double deficient mice models.
- Analyzed the expression of MAG-positive immature oligodendroglia at different developmental stages.
- Compared cellular populations between wild-type and genetically modified mice.
Main Results:
- MBP-deficient mice exhibited reduced MAG-positive immature oligodendroglia during early myelination.
- An increase in these immature glia was observed in adult MBP-deficient mice.
- MBP/Fyn-double deficiency showed a moderate increase in immature glia, less severe than MBP deficiency alone.
- Results suggest MBP regulates MAG expression in oligodendroglia, involving Fyn kinase.
Conclusions:
- MBP is essential for the regulation of MAG expression in oligodendroglia during early myelination.
- Fyn kinase is implicated in the MBP-dependent regulation of MAG.
- A molecule other than MAG might be responsible for initiating the myelination process.