Strain Name: |
SWR/J |
|---|---|
Stock Number: |
000689 |
Availability: | Level 3 |
General Terms and Conditions |
| Former Name |
SWR/J-Pde6brd1 (Changed: 19-MAR-08
) |
| Strain Common Names | swiss; SW; |
| Genes & Alleles | Hc; Hc0; Pde6b; Pde6brd1; |
Product Information
Strain Details
Type Inbred Strain Additional information on Inbred Strains. Mating System Sibling x Sibling (Female x Male) Species laboratory mouse H2 Haplotype q2 (see, Fischer Lindahl K 1997 and Shen FW 1982) Generation F229 (03-JAN-08) Appearance
albino
Related Genotype: A/A Tyrc/TyrcImportant Note
This strain is homozygous for the retinal degeneration allele Pde6brd1. See article "Genetic Background Effects: Can Your Mice See?", JAX Notes Spring 2002, No. 485.Strain Description
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 prominant 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/LtJ 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).Strain Development
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+.
Gene & Allele Details
| Allele Symbol | Hc0 | ||
|---|---|---|---|
| Allele Name | deficient | ||
| Common Name(s) | C5-; C5-d; C5-def; C5-deficient; hco; | ||
| Gene Symbol and Name | Hc, hemolytic complement | ||
| Chromosome | 2 | ||
| Gene Common Name(s) | C5; C5a; CPAMD4; FLJ17816; FLJ17822; He; MGC142298; RGD1561905; | ||
| General Note |
This is an allele characteristic of various inbred mouse strains including the following: A/HeJ, 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, AKR/J, DBA/2J, NZB/B1NJ, 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. [MGI Ref ID J:23983] | ||
| Allele Symbol | Pde6brd1 | ||
| Allele Name | retinal degeneration 1 | ||
| Common Name(s) | rd; rd-1; rd1; rodless retina; | ||
| Gene Symbol and Name | Pde6b, phosphodiesterase 6B, cGMP, rod receptor, beta polypeptide | ||
| Chromosome | 5 | ||
| Gene Common Name(s) | CSNB3; PDEB; Pdeb; RP40; nmf137; phosphodiesterase, cGMP, rod receptor, beta polypeptide; r; rd; rd-1; rd1; rd10; retinal degeneration; retinal degeneration 1; retinal degeneration 10; | ||
| 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 also been identified in all rd1 strains of mice. A specific degradation of mutant transcript during or after pre-mRNA splicing is suggested. [MGI Ref ID J:11513] [MGI Ref ID J:4366] [MGI Ref ID J:51361] | ||
Colony Maintenance
| Diet Information | LabDiet® 5K52/5K67 |
|---|
Related Strains
SWR Strains
001900 SWR/Bm View SWR Strains (1 strain)
000645 A/HeJ 000646 A/J 000647 A/WySnJ 000648 AKR/J 000460 B10.D2-Hc0 H2d H2-T18c/o2SnJ 000461 B10.D2-Hc0 H2d H2-T18c/oSnJ 000657 CE/J 000671 DBA/2J 007048 DBA/2J-Gpnmb+/SjJ 001800 FVB/NJ 001491 FVB/NMob 000674 I/LnJ 001303 NOD.CB17-Prkdcscid/J 001976 NOD/ShiLtJ 000684 NZB/BlNJ 000682 RF/J 000688 ST/bJ
000470 AK.M-H2m H2-T18a/nSnJ 005308 B10.Cg-H2d Tg(TcraCl4,TcrbCl4)1Shrm/ShrmJ 000463 B10.D2-Hc1 H2d H2-T18c/nSnJ 003147 B10.D2-Hc1 H2d H2-T18c/nSnJ-Tg(DO11.10)10Dlo/J 004306 NOD.CBALs-Hc1/LtJ
004297 B6.CXB1-Pde6brd10/J 002802 C3.BLiA Pde6b+-Krd/J 001979 C3A.BLiA-Pde6b+.O20-Prph2Rd2/J 001912 C3A.BLiA-Pde6b+/J 003648 C3Sn.BLiA-Pde6b+/Dn 004766 C57BL/6J-Pde6brd1-2J/J 004828 FVB.129P2-Pde6b+ Tyrc-ch/AntJ 004808 STOCK Mapttm1(EGFP)Klt Tg(MAPT)8cPdav/J
Phenotypic Data
Mouse Phenome Database
Festing Inbred Strain Characteristics: SWR
Additional Web Information
Genetic Quality Control Annual Report
JAX Notes, April 1988; 433. H-2 Haplotypes of Mice from Jackson Laboratory Production Colonies.
JAX Notes, Spring 1999; 477. Control Strains for NOD/LtJ Mice in Diabetes Research.
JAX Notes, Spring 2002; 485. Genetic Background Effects: Can Your Mice See?
Animal Health Reports
Room Number MP13
Research Applications
This mouse can be used to support research in many areas including:
Hc0 relatedCancer Research
Increased Tumor Incidence (Mammary Gland Tumors)
Increased Tumor Incidence (Other Tissues/Organs: lung)
Cardiovascular Research
Diet-Induced Atherosclerosis (Susceptible)
Developmental Biology Research
Lymphoid Tissue Defects (hematopoietic defects)
Diabetes and Obesity Research
Type 1 Diabetes (IDDM) Analysis Strains (Related Inbred Strains)
Immunology and Inflammation Research
Autoimmunity (experimental allergic encephalomyelitis (EAE))
Immunodeficiency (specific complement deficiency)
Research Tools
General Purpose
Immunology and Inflammation Research (specific complement deficiency) (C5 complement)
Sensorineural Research
Retinal Degeneration (Homozygous for Pde6brd1)
Pde6brd1 relatedImmunology and Inflammation Research
Immunodeficiency (specific complement deficiency)
Research Tools
Immunology and Inflammation Research (specific complement deficiency) (C5 complement)
Mouse/Human Gene Homologs
retinitis pigmentosa, autosomal recessive
Sensorineural Research
Retinal Degeneration
References
Selected Reference(s)
Additional ReferencesDeringer MK. 1970. Mammary tumors in strains BL-LyDe and SWR-LyDe mice. J Natl Cancer Inst 45(2):215-8. [PubMed: 4324608] [MGI Ref ID J:69927]
Fischer Lindahl K. 1997. On naming H2 haplotypes: functional significance of MHC class Ib alleles. Immunogenetics 46(1):53-62. [PubMed: 9148789] [MGI Ref ID J:41130]
Jiao S; Cole TG; Kitchens RT; Pfleger B; Schonfeld G. 1990. Genetic heterogeneity of plasma lipoproteins in the mouse: control of low density lipoprotein particle sizes by genetic factors. J Lipid Res 31(3):467-77. [PubMed: 1971301] [MGI Ref ID J:15484]
Kirk EA; Moe GL; Caldwell MT; Lernmark JA; Wilson DL; LeBoeuf RC. 1995. Hyper- and hypo-responsiveness to dietary fat and cholesterol among inbred mice: searching for level and variability genes. J Lipid Res 36(7):1522-32. [PubMed: 7595076] [MGI Ref ID J:28648]
Kutscher CL; Miller DG. 1974. Age-dependent polydipsia in the SWR-J mouse. Physiol Behav 13(1):71-9. [PubMed: 4850464] [MGI Ref ID J:33646]
Kutscher CL; Miller M; Schmalbach NL. 1975. Renal deficiency associated with diabetes insipidus in the SWR/J mouse. Physiol Behav 14(6):815-8. [PubMed: 1187837] [MGI Ref ID J:25303]
Kutscher CL; Schmalbach NL. 1975. Effects of water deprivation, NaCl injection, and seven aversive taste stimuli on drinking in two normal mouse strains and one with diabetes insipidus. Physiol Behav 15(6):659-67. [PubMed: 1226406] [MGI Ref ID J:25302]
Levine S; Sowinski R. 1973. Experimental allergic encephalomyelitis in inbred and outbred mice. J Immunol 110(1):139-43. [PubMed: 4631068] [MGI Ref ID J:24660]
Lindsey JW. 1996. Characteristics of initial and reinduced experimental autoimmune encephalomyelitis. Immunogenetics 44(4):292-7. [PubMed: 8753860] [MGI Ref ID J:35147]
Lynch CJ. 1969. The so-called Swiss mouse. Lab Anim Care 19(2):214-20. [PubMed: 4240230] [MGI Ref ID J:24849]
Nishina PM; Wang J; Toyofuku W; Kuypers FA; Ishida BY; Paigen B. 1993. Atherosclerosis and plasma and liver lipids in nine inbred strains of mice. Lipids 28(7):599-605. [PubMed: 8355588] [MGI Ref ID J:13267]
Ortman RA; Holderbaum D; Qu XM; Banerjee S; Haqqi TM. 1994. BUB/BnJ (H-2q) is a TCR deletion mutant mouse strain (TCR V beta a, KJ16-) that is susceptible to type II collagen-induced arthritis. J Immunol 152(8):4175-82. [PubMed: 8144978] [MGI Ref ID J:17601]
Osman GE; Hannibal MC; Anderson JP; Cheunsuk S; Lasky SR; Liggitt HD; Ladiges WC; Hood LE. 1999. T-cell receptor vbeta deletion and valpha polymorphism are responsible for the resistance of SWR mouse to arthritis induction. Immunogenetics 49(9):764-72. [PubMed: 10398803] [MGI Ref ID J:109896]
Osman GE; Jacobson DP; Li SW; Hood LE; Liggitt HD; Ladiges WC. 1997. SWR: an inbred strain suitable for generating transgenic mice. Lab Anim Sci 47(2):167-71. [PubMed: 9150496] [MGI Ref ID J:40533]
Paigen B. 1995. Genetics of responsiveness to high-fat and high- cholesterol diets in the mouse. Am J Clin Nutr 62(2):458S-462S. [PubMed: 7625360] [MGI Ref ID J:28248]
Paigen B; Ishida BY; Verstuyft J; Winters RB; Albee D. 1990. Atherosclerosis susceptibility differences among progenitors of recombinant inbred strains of mice. Arteriosclerosis 10(2):316-23. [PubMed: 2317166] [MGI Ref ID J:22615]
Paigen B; Morrow A; Brandon C; Mitchell D; Holmes P. 1985. Variation in susceptibility to atherosclerosis among inbred strains of mice. Atherosclerosis 57(1):65-73. [PubMed: 3841001] [MGI Ref ID J:109950]
Serreze DV; Leiter EH. 1988. Defective activation of T suppressor cell function in nonobese diabetic mice. Potential relation to cytokine deficiencies. J Immunol 140(11):3801-7. [PubMed: 2897395] [MGI Ref ID J:27617]
Shen FW; Chorney MJ; Boyse EA. 1982. Further polymorphism of the Tla locus defined by monoclonal TL antibodies. Immunogenetics 15(6):573-8. [PubMed: 7106865] [MGI Ref ID J:6828]
Price and Supply Information
| Strain Name: | SWR/J |
| Stock Number: | 000689 |
Price Details
IMPORTANT NOTE: Prices are based on shipping destination. To view prices, select your shipping destination.
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Supply Details
| Standard Supply | Level 3. Up to 50 mice. Larger quantities or custom orders arranged upon request. |
|---|---|
| Supply Notes |
Shipped at a specific age in weeks. Mice at a precise age in days, littermates and retired breeders are also available. Strains that must be genotyped are not available until five to seven weeks of age. Genomic DNA is available for this strain from the Mouse DNA Resource. |
| Licensing | See General Terms and Conditions below |
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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.Ordering and Purchasing Information
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