These mice carry an ENU-induced mutation characterized by reduced forelimb grip strength and subtle gait abnormalities.
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 were originally detected by reduced (<= 2 s.d. B6 mean) forelimb grip strength at 12 weeks of age. Subsequent observations revealed subtle abnormalities in their gait that can be detected at approximately 4 weeks of age (average on-set 4.3+/-0.75 weeks; n=33). In the interest of expediting availability, only the early visible phenotype was pursued.
Standard pathology work-up on two mutants (31 or 282 days of age)did not reveal any abnormalities. Whole muscle mounts of the hind limb stained with fluorescent-labeled bungarotoxin, SV2, and SMI 31 revealed no abnormalities of neuromuscular junctions. Additional pathology on brain, spinal cord, muscle and eyes performed on three other mutants (24 or 114 days of age) revealed retinal dysplasia in the older mutant. The eyes of all other mutants appeared normal.
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, 62|
|Allele Type||Chemically induced (ENU)|
|Gene Symbol and Name||nmf62, neuroscience mutagenesis facility, 62|
|Strain of Origin||C57BL/6J|
|Molecular Note||This phenotypic mutant was identified in an ENU mutagenesis screen.|