These mice carry an ENU-induced mutation and exhibit progressive loss of hind limb control.
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 +
Younger animals show intermittent hind limb spasms and curled front or hind limb toes, however, the phenotype becomes more severe with age; mutants are then barely able to use their hind limbs which frequently remain closely clasped to their body. While moving or sitting, hind limbs may also turn flaccid, and occasionally cross over or become intertwined. When picked up by their tail, mutants of any age keep hind limbs closely clasped to their body; the hind limb flexor reflex is quite brisk. The phenotype becomes observable at 4.6+/-2.2 weeks of age (average; n=36); it might be possible to maintain a colony through regular breeding, however some mutants were found to be unproductive, and age or severity of phenotype expression may have contributed to that.
Standard pathology work-up on two mutants (10 or 31 days of age) revealed thin cerebellar folia in the older mouse; no other abnormalities were noted in either animal. Whole muscle mounts of the hind limb of an additional mutant (59 days of age) stained with fluorescent-labeled bungarotoxin, SV2, or SMI 31 also revealed no abnormalities.
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, 418|
|Allele Type||Chemically induced (ENU)|
|Gene Symbol and Name||nmf418, neuroscience mutagenesis facility, 418|
|Strain of Origin||C57BL/6J|
|Molecular Note||This phenotypic mutation was identified in an ENU mutagenesis screen.|