These mice carry an ENU-induced mutation resulting in ataxia.
The Jackson Laboratory cannot guarantee that cryorecovery of strains from the discontinued NIH-funded Neuroscience Mutagenesis Facility (NMF) will be successful or that the anticipated phenotype or genotype will be obtained. The cryorecovery fee for this effort will not be refunded or prorated if the recovery is unsuccessful or is in any way unsatisfactory. Genotyping will be the responsibility of the Purchaser.Read More +
The mutants have splayed hind limbs, and show body tremor and trunk swaying at rest, which intensify during movement. They stagger forward, swaying intensely although adult mutants usually manage to keep on their feet; younger mutants lean and frequently fall to the side. Their hind limbs are lifted high when walking, and also show occasional spasms. When lifting the mice by their tail, hind legs remain close to their body. The average onset of this phenotype is at 3 weeks of age (3.6 +/- 0.6 weeks; n=60). Mapping results place the mutation into a relative gene-poor region in the vicinity of the glutamate receptor, metabotropic 1 (Grm1). Standard pathology work-up on two mutants (29 days of age) revealed no abnormalities. A colony has to be maintained through ovarian transplants and heterozygote x heterozygote matings.
This phenotypic deviant was generated by ethylnitrosourea (ENU) mutagenesis in C57BL/6J males (Stock No. 000664), in the Neuroscience Mutagenesis facility at The Jackson Laboratory. Mutagenized males were crossed to C57BL/6J females; G3 descendants of the mutagenized males were selected for neurological impairment.
|Allele Name||neuroscience mutagenesis facility, 373|
|Allele Type||Chemically induced (ENU)|
|Gene Symbol and Name||Grm1, glutamate receptor, metabotropic 1|
|Strain of Origin||C57BL/6J|
|Molecular Note||This phenotypic mutation was identified in an ENU mutagenesis screen. A T480C transition has been identified causing a I160T amino acid substitution.|