Mice homozygous for this targeted mutation of mouse Sod2 (superoxide dismutase 2, mitochondrial) are embryonic lethal. Crosses with DBA/2J inbred mice enhance homozygous viability and produce animals exhibiting severe wasting and progressive ataxia.
Dr. Russell Lebovitz, SUMA Partners
Genetic Background | Generation |
---|---|
|
Allele Type | Gene Symbol | Gene Name |
---|---|---|
Targeted (Null/Knockout) | Sod2 | superoxide dismutase 2, mitochondrial |
Original studies of this strain, first published in 1996, describe homozygous animals that died within 21 days of birth and exhibited several novel pathogenic phenotypes including severe anemia, degeneration of neurons in the basal ganglia and brainstem, progressive motor disturbances, and myocardial injury. Applications included studies of idiopathic cardiomyopathy and sporadic motor neuron disease.
It has been found, however, that mice homozygous for the Sod2tm1Leb mutation on the current C57BL/6 genetic background (backcross generation N5+25 - July, 2017) are embryonic lethal. In one recent study, heterozygote x heterozygote crosses produced no homozygous mutants at P0-P1 (0/40 pups; unpublished).
Improved homozygous viability has been demonstrated in matings of B6.129S7-Sod2tm1Leb/J (Stock# 002973) mutant mice with DBA/2J inbred animals (Stock# 000671). Intercrosses of F1 animals yield F2 homozygous pups at a lower-than-predicted Mendelian percentage, but they have a median survival time of 12 days. The C57BL/6-DBA/2J (B6D2F2) mixed background mutant animals (not currently offered by The Jackson Laboratory) display severe wasting and progressive ataxia. The heart and brain have not been examined histologically. This data has not been published (July, 2017).
The Sod2tm1Leb targeted mutation was made by Dr. Russell Lebovitz. A 1.5 Kb HindIII fragment containing exons 1 and 2 of the Sod2 gene, as well as approximately 500bp immediately 5' of exon 1, was replaced with a human hypoxanthine phosphoribosyltransferase minigene driven by the phosphoglycerate kinase promoter. The transcription and translation start sites, the mitochondrial targeting sequence, and one of the three histidines that bind directly to the manganese cofactor, have been eliminated. The 129S7/SvEvBrd-Hprtb-m2-derived AB 2.1 ES cell line was used. The Sod2tm1Leb targeted mutation was initially backcrossed more than 5 times to C57BL/6 mice prior to arrival at The Jackson Laboratory. A further 25 generations of backcrossing to C57BL/6J have subsequently occurred (July, 2017).
Allele Name | targeted mutation 1, Russell M Lebovitz |
---|---|
Allele Type | Targeted (Null/Knockout) |
Allele Synonym(s) | Sod2-; SOD2m1BCM; Sod2mlbcm |
Gene Symbol and Name | Sod2, superoxide dismutase 2, mitochondrial |
Gene Synonym(s) | |
Strain of Origin | 129S7/SvEvBrd-Hprtb-m2 |
Chromosome | 17 |
Molecular Note | A human HPRT minigene driven by the PGK promoter replaced exons 1 and 2, and sequences approximately 500 bp immediately 5' of exon 1. The replaced region encodes the transcription and translation start sites, the mitochondrial targeting sequence, and one of three histidines that bind directly to the manganese cofactor. Northern blot analysis of brain did not detect mRNA in homozygous mutant mice. Enzyme activity assays of heart did not detect active protein in homozygous mutant mice. |
Mutations Made By | Dr. Russell Lebovitz, SUMA Partners |
This strain is maintained by mating heterozygotes (female or male) with C57BL/6J inbred mice. Homozygotes are embryonic lethal.
When using the SOD2m1BCM mouse strain in a publication, please cite the originating article(s) and include JAX stock #002973 in your Materials and Methods section.
Facility Barrier Level Descriptions
Service/Product | Description | Price |
---|---|---|
Heterozygous or Wild-type for Sod2<tm1Leb> |
Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.
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.
What information were you hoping to find through your search?
How easy was it to find what you were looking for?
We may wish to follow up with you. Enter your email if you are happy for us to connect and reachout to you with more questions.
Please Enter a Valid Email Address
Thank you for sharing your feedback! We are working on improving the JAX Mice search. Come back soon for exciting changes.