These mice carry an ENU-induced mutation and are characterized by ataxic episodes.
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 lose function intermittently, i.e. both or one or the other hind leg may lag behind, or may be stretched to the side or front during movement (average onset 4.6 +/- 0.8 weeks of age; n=15). These episodes usually last less than a minute, and the mice then move around quite normally. Front limbs appear to be affected to a lesser degree. When the mutants are lifted up by their tail, the hind legs come together and point down- or backwards. Because of the phenotypic similarity to that observed following mutations of the Clcn1 (Chloride channel 1) gene, complementation tests between NMF310 and Clcn1adr-mto were conducted. The results of heterozygous x heterozygous matings (NMF310 x Stock No. 001265 BALB/cByj-Clcn1adr-mto-2J/J), i.e. 6 affected mice in a total of 29 progeny, suggest that NMF310 represents an allele of Clcn1. Standard pathology work-up on one mutant (88 days of age) revealed no abnormalities. Mutants do not breed and the colony has to be 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. Mutagenized males were crossed to C57BL/6J females; G3 descendants of the mutagenized males were selected for neurological impairment.
|Allele Name||myotonia 6 Jackson|
|Allele Type||Chemically induced (ENU)|
|Allele Synonym(s)||Clcn1nmf310; neuroscience mutagenesis facility 310; NMF310|
|Gene Symbol and Name||Clcn1, chloride channel, voltage-sensitive 1|
|Strain of Origin||C57BL/6J|
|General Note||The hind limbs of these mutants appear to lose function intermittently, i.e. both or one or the other hind leg may lag behind, or may be stretched to the side or front during movement. These episodes usually last less than a minute, and the mice then move around quite normally. Front limbs appear to be affected to a lesser degree. When the mutants are lifted up by their tail, the hind legs come together and point down- or backwards. The mutants do not breed and the colony has to be maintained through ovarian transplants.|
|Molecular Note||Complementation tests between NMF310 and Clcn1adr-mto were conducted. The results of heterozygous x heterozygous matings (NMF310 x BALB/cByj-Clcn1adr-mto2J), i.e. 6 affected mice in a total of 29 progeny, suggest that NMF310 represents an allele of Clcn1.|
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