These Mag knock-out mice exhibit a partial impairment of organization of the periaxonal region, and mutant animals show a subtle intention tremor.
Dr. John Roder, University of Toronto
Mice homozygous for the Magtm1Rod targeted mutation are viable and fertile. Mag had previously been thought to be necessary for myelin formation. However in the homozygous mutant the degree of myelination and its compaction are normal. Finer motor coordination abilities are significantly affected in the homozygous mutant and they exhibit a subtle intention tremor. The organization of the periaxonal region is partially impaired with the periaxonal cytoplasmic collar frequently missing in optic nerve, cervical spinal cord, and ventral roots. Later in life, beginning at 6 months, oligodendrocytes degenerate. This strain may serve as a model for some aspects of multiple sclerosis. MAG also tranduces a signal to axons. Therefore, axons in the MAG-deficient mice are smaller in calliber due to the aberrant phosphorylation of neurofilaments. MAG has also been shown to be an inhibitor of nerve regeneration.
The Mag-deficient strain was developed in the laboratory of Dr. John Roder at the Samuel Lunenfeld Research Institute in Toronto.
|Allele Name||targeted mutation 1, John Roder|
|Allele Type||Targeted (Null/Knockout)|
|Gene Symbol and Name||Mag, myelin-associated glycoprotein|
|Strain of Origin||(129X1/SvJ x 129S1/Sv)F1-Kitl+|
|Molecular Note||A neomycin resistance cassette was inserted into exon 5 of the gene. Mutant mice showed a complete lack of mRNA and protein in the central nervous system for the targeted gene. Nerves from the peripheral nervous system also lacked protein for the targeted gene.|
|Mutations Made By|| |
Dr. John Roder, University of Toronto
This strain is maintained by homozygous sibling matings. Expected coat color from breeding:White Bellied Agouti
When using the MAG KO mouse strain in a publication, please cite the originating article(s) and include JAX stock #002403 in your Materials and Methods section.
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