SWR/J mice are used widely in research as a general purpose strain. Aging mice exhibit a high incidence of lung and mammary gland tumors. They also develop extreme polydipsia and polyuria (nephrogenic diabetes insipidus) with increasing age. SWR/J mice are highly susceptible to experimental allergic encephalomyelitis. SWR/J mice show an intermediate susceptibility to developing atherosclerotic aortic lesions following an atherogenic diet. SWR/J mice are useful for creation of transgenic mice because they are high responders to exogenous hormones and have large and prominent pronuclei with good resistance to lysis following microinjection. SWR/J mice appear to be the only inbred carrying the allele Soaa (Taster) characterized by avoidance of sucrose octaacetate solutions at low concentrations.Read More +
This strain is homozygous for the retinal degeneration allele Pde6brd1.
SWR/J mice are used widely in research as a general purpose strain. Aging mice exhibit a high incidence of lung and mammary gland tumors. They also develop extreme polydipsia and polyuria (nephrogenic diabetes insipidus) with increasing age. SWR/J mice are highly susceptible to experimental allergic encephalomyelitis (EAE). Germline deletion of about 50% of T-cell receptor V beta-chain gene segments and a T-cell receptor V alpha polymorphism are responsible for the resistance of SWR/J mice to collagen type II-induced arthritis. SWR/J mice show an intermediate susceptibility to developing atherosclerotic aortic lesions (1670 to 1690 um2 atherosclerotic aortic lesions/aortic cross-section) following 14 weeks on an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat). SWR/J mice have been recommended for generation and propogation of transgenic mice because they are high responders to exogenous hormones, have large and prominent pronuclei with good resistance to lysis following microinjection, and are genetically well-defined. SWR/J mice may also be used as controls for comparison to the autoimmune diabetic NOD/ShiLtJ mice (Stock No. 001976), especially for experiments examining the aberrant immune functions of NOD/ShiLtJ mice. Both NOD and SWR/J mice are derived from Swiss mice. SWR/J are in some cases more suitable than random bred Swiss ICR mice because of their genetic uniformity. Unlike NOD/ShiLtJ mice they are not immunocompromised, and they are genetically very different from NOD. SWR/J mice appear to be the only inbred carrying the allele Soaa (Taster) characterized by avoidance of sucrose octaacetate solutions at low concentrations (< 10-3M).
The SWR inbred strain was developed by Clara J Lynch at The Rockefeller Institute who obtained swiss mice from A. de Coulon of Lausanne, Switzerland and began inbreeding around 1926. This strain was transferred to Raymond Parker at the University of Toronto who supplied them to The Jackson Laboratory in 1947 at F28+. In 1996 embryos were cryopreserved when this strain was at inbreeding generation F191.
|Allele Synonym(s)||C5-; C5-d; C5-def; C5-deficient; HcHfib2; hco|
|Gene Symbol and Name||Hc, hemolytic complement|
|Strain of Origin||multiple strains|
|General Note|| |
This is an allele characteristic of various inbred mouse strains including the following: A/HeJ, A/J, AKR/J, DBA/2J, NZB/B1NJ, SWR/J, B10.D2/oSnJ
Hc was identified as a candidate gene for Abhr2 in a microarray analysis of lung mRNA from A/J, C3H/HeJ, and (A/J x C3H/HeJ)F1 x A/J backcross animals. Hc genotype shows statistically significant correlation to allergen-induced bronchial hyperresponsive phenotype. The A/J allele contains a 2 bp deletion resulting in deficient Hc mRNA and protein production and is associated with susceptibility to allergen-induced bronchial hyperresponsiveness. (J:108211)
|Molecular Note||A 2 base "TA" deletion at positions 62 and 63 of an 83 base pair exon near the 5' end of the gene is found in the following mouse strains: A/HeJ, A/J, AKR/J, DBA/2J, I/LnJ, KK/HlJ, MOLF/EiJ, NZB/B1NJ, RF/J, ST/bJ SWR/J, B10.D2/oSnJ. The consequence of this deletion is the creation of a stop codon starting four bases after the deletion. A truncated product of 216 amino acids is predicted as a result although contradictory reports exist that a larger pro-C5 protein may be synthesized. Nevertheless, macrophages from mouse strains carrying this allele do not secrete complement 5.|
|Allele Synonym(s)||Disc1129S6; Disc1delta6|
|Gene Symbol and Name||Disc1, disrupted in schizophrenia 1|
|Strain of Origin||various|
|General Note||This deletion appears in multiple strains of the 129 superfamily, 101/RI, BTBR T+ tf/J, LP/J, FVB/NJ, SJL/J, SWR/J and DDY/JclSidSeyFrkJ (J:111837, J:195189).|
|Molecular Note||A 25 bp deletion in exon 6 causes a frame shift in the reading frame, resulting in 13 novel amino acids and a premature stop codon in exon 7.|
|Allele Name||d variant|
|Allele Type||Not Applicable|
|Allele Synonym(s)||ah; Ahd; Ahk; Ahhn; AhRd; in|
|Gene Symbol and Name||Ahr, aryl-hydrocarbon receptor|
|Strain of Origin||Not Applicable|
|General Note|| |
Strain of origin - this allele was found in DBA/2J, AKR/J, 129, SWR, RF, NZB strains
|Molecular Note||This allele encodes a 104 kDa receptor that is stabilized by molybdate and has an affinity for ligand 10-100 fold lower than that of the receptor produced by the C57BL/6J allele. PCR sequencing of cDNA revealed ten nucleotide differences between the coding sequences of the DBA/2J and C57BL/6J receptors. Five of the ten differences would cause amino acid changes. One of these, an apparent T to C transition replaces the opal termination codon in the C57BL/6J allele with an arginine codon in the DBA/2J allele. This change would extend translation of the DBA/2J mRNA by 43 amino acids, accounting for the larger size of the peptide produced by this allele (104 kDa vs 95 kDa for the C57BL/6J allele). A second T to C transition changes a leucine codon in the C57BL/6J allele to a proline codon in the DBA/2J allele, and would likely change secondary structure of the peptide and thus ligand affinity.|
|Allele Name||retinal degeneration 1|
|Allele Synonym(s)||Pdebrd1; rd; rd1; rd-1; rodless retina|
|Gene Symbol and Name||Pde6b, phosphodiesterase 6B, cGMP, rod receptor, beta polypeptide|
|Strain of Origin||various|
|General Note||The following inbred strains are known to be homozygous for Pde6b |
|Molecular Note||Two mutations have been identified in rd1 mice. A murine leukimia virus (Xmv-28) insertion in reverse orientation in intron 1 is found in all mouse strains with the rd1 phenotype. Further, a nonsense mutation (C-to-A transversion) in codon 347 that results in a truncation eliminating more than half of the predicted encoded protein, including the catalytic domain, has been identified in all rd1 strains of mice. A specific degradation of mutant transcript during or after pre-mRNA splicing is suggested.|
When using the SWR/J mouse strain in a publication, please include JAX stock #000689 in your Materials and Methods section.
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