STOCK Mag^tm1Rod/J

Stock number: 002403
Product name: MAG KO
Research areas: Neurobiology Research

Description

These Mag knock-out mice exhibit a partial impairment of organization of the periaxonal region, and mutant animals show a subtle intention tremor.

Detailed description

Mice homozygous for the Mag^tm1Rod 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.

Development

The Mag-deficient strain was developed in the laboratory of Dr. John Roder at the Samuel Lunenfeld Research Institute in Toronto.

Allele

Symbol: Mag^tm1Rod
Name: targeted mutation 1, John Roder
MGI accession ID: MGI:1857216
Generation method: Targeted
Attributes: Null/Knockout
Marker symbol: Mag
Marker name: myelin-associated glycoprotein
Chromosome: 7
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.