These mice carry an ENU-induced mutation characterized by an unsteady gait, labored breathing, and progressive wasting.
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 +
Mutants are small and show reduced grip strength (< 2 S.D. B6 mean) at 12 weeks of age. At 16 weeks of age they show an unsteady gait and labored breathing. By 17 weeks of age the mice appear extremely wasted. Standard pathology work-up on three mutants revealed mild myopathy in all muscles characterized by scattered small muscle fibers often with central nuclei. Whole muscle mounts of hind limb stained with flurorescent-labeled bungarotoxin, SV2 and SMI 31 revealed no abnormalities of neuromuscular junctions. GFAP immunohistochemistry of brain and spinal cord showed gliosis of white matter in medulla and spinal cord. In dorsal columns of spinal cord the sensory tracts were quite severely gliotic, but the corticospinal tract was normal. A few dystrophic axons were observed in low lumbar spinal cord.
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, 65|
|Allele Type||Chemically induced (ENU)|
|Gene Symbol and Name||nmf65, neuroscience mutagenesis facility, 65|
|Strain of Origin||C57BL/6J|
|Molecular Note||This phenotypic mutant was identified in an ENU mutagenesis screen.|
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