These mice carry an ENU-induced mutation shown to be a new allele of Scn8a and characterized by functional lose of hind limbs bilaterally.
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) | Scn8a | sodium channel, voltage-gated, type VIII, alpha |
The mutants lose function of hind limbs bilaterally between 13-18 days (mean 15.25 +/-.2 days; n=13) and die between 3 and 5 weeks of age.
A series of complementation tests was performed to show that NMF2 is an allele of Scn8a 2 matings between NMF5/+ and NMF2/+ resulted in 2 affected mice in a total of 13 progeny, and since NMF5 has been shown to be an allele of NMF58, NMF2 can also be regarded as an allele of NMF58. Recent sequencing data confirmed the allelic relationship of NMF58 and Scn8a, and therefore also those of NMF2, NMF5, and Scn8a (Mammalian Genome, 15,4, 2004). Standard pathology work-up on 4 mutants (age 18-19 days) showed no muscle atrophy or necrosis. Additional histology of hindlimb muscles showed no evidence of reinnervation/regeneration and normal neuromuscular junction morphology in all mice. One mutant had severe hydrocephaly. Standard eye histology on one mutant and one control littermate (age 16 days) showed no abnormalities. Mutants are small in size.
Mutants of either gender have been produced, however homozygotes are not viable.
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 | 4 Jackson |
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Allele Type | Chemically induced (ENU) |
Allele Synonym(s) | neuroscience mutagenesis facility, 2; NMF2; Scn8anmf2 |
Gene Symbol and Name | Scn8a, sodium channel, voltage-gated, type VIII, alpha |
Gene Synonym(s) | |
Strain of Origin | C57BL/6J |
Chromosome | 15 |
Molecular Note | This phenotypic mutant was identified in an ENU mutagenesis screen. A complementation test between nmf2 and Scn8anmf5 revealed that nmf2 is a new allele of Scn8a. Sequence analysis demonstrated that an A-to-C transversion mutation occurred in the coding sequence that is predicted to change asparagine 1370 to threonine. This conserved residue is within the S5-S6 pore loop of transmembrane domain 3. |
When using the nmf2 mouse strain in a publication, please cite the originating article(s) and include JAX stock #004102 in your Materials and Methods section.
Facility Barrier Level Descriptions
Service/Product | Description | Price |
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Unknown for Scn8a<4J> |
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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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