These mice carry an ENU-induced mutation and exhibit mild nerve degeneration in the hind limbs of some mutants.
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 hind limbs of these mutants appear to be weak, and unable to sufficiently support the posterior part of the mutants' body, which remains low; at times hind limbs remain longer on the ground during movement, or are moved simultaneously (ataxia) resulting in a less well coordinated gait than that of unaffected mice. However, the mutants move around quite well. Body tremor is observable during movement; the hind limb withdrawl (flexor) reflex is brisk. On-set of this phenotype is at wean (average on-set 4.3+/- 1.7 weeks of age; n=15). Standard pathology work-up on three mutants (22-38 days of age) revealed mild nerve degeneration in the hind limbs of two of the three mice. The colony is maintained through ovarian transplants.
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.
|Allele Name||neuroscience mutagenesis facility, 419|
|Allele Type||Chemically induced (ENU)|
|Gene Symbol and Name||nmf419, neuroscience mutagenesis facility, 419|
|Strain of Origin||C57BL/6J|
|Molecular Note||This phenotypic mutation was discovered in an ENU mutagenesis screen.|