These mice carry an ENU-induced allelic mutation of the Dst (Dystonin) gene resulting in ataxia.
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 +Genetic Background | Generation |
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Allele Type | Gene Symbol | Gene Name |
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Chemically induced (ENU) | Dst | dystonin |
The mutants are small and their movement ability is severely limited. They move forward mainly by 'robbing' on their belly, since their front limbs are usually bent at the elbow, and their hind limbs lag behind. No muscle tonus is apparent in either front- or hind limbs upon gently pulling a limb, indicating flaccid paralysis of these limbs. A righting reflex is present only in rudimentary form, i.e. it may take a few seconds before the animal can righten itself from a back-lying position; when picked up by their tail, front- and hind limbs come together, the former are pulled backward, the latter move forward.
Because of phenotypic similarity to dystonia musculorum, complementation tests with Dstdt-J/J (JR# 0211) have been performed to determine if NMF339 represents an allele of Dst (Dystonin). Four heterozygote matings (NMF339 x Dstdt-J/J, n=2; Dstdt-J/J) x NMF339, n=2) produced 8 mutants in a total of 30 progeny, suggesting that NMF339 indeed represents a new allele of Dstdt-J.
Standard pathology work-up performed on three mutants at 19 (n=1) or 21 (n=2) days of age showed central chromatolysis in neurons of the brain stem and spinal cord, and dystrophic axons. Myelin degeneration, characterized by myelin figures in the cytoplasm of neurons was noted in the peripheral nerves; small muscle fibers and hypoplastic bone marrow (at 21 days of age) were also observed.
These mice are affected at a young age (average onset 2.8 weeks +/- 1; n=21), and the colony had 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 | dystonia musculorum 37, Jackson |
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Allele Type | Chemically induced (ENU) |
Allele Synonym(s) | Dstnmf339; neuroscience mutagenesis facility, 339; NMF339 |
Gene Symbol and Name | Dst, dystonin |
Gene Synonym(s) | |
Strain of Origin | C57BL/6J |
Chromosome | 1 |
Molecular Note | This mutation was discovered in an ENU mutagenesis screen and was shown to be an allele of Dst by its failure to complement the dystonia musculorum Jackson mutation. |
When using the dystonia musculorum(37J) mouse strain in a publication, please cite the originating article(s) and include JAX stock #005560 in your Materials and Methods section.
Facility Barrier Level Descriptions
Service/Product | Description | Price |
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Unknown for Dst<dt-37J> |
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The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project. We do not guarantee breeding performance and therefore suggest that investigators order more than one breeding pair to avoid delays in their research.
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