Strain Name: |
NON/ShiLtJ |
|---|---|
Stock Number: |
002423 |
Availability: | Repository- Live |
General Terms and Conditions |
| Former Name |
NON/LtJ (Changed: 23-FEB-07
) |
|
Non-obese Non-diabetic (Changed: 15-DEC-04
) | |
| Genes & Alleles | 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 nb1 Generation F124 (05-DEC-07) 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
Although closely related to NOD mice, NON mice contain a diabetes resistant MHC haplotype (H2nb1 = Kb, Anb1, Ek, Db). The name was derived from "Non-Obese Non-diabetic"; however, NON/ShiLtJ mice should not be considered "normal." They carry the retinal degeneration (Pde6b) mutation and exhibit certain tendencies toward autoimmune disease. This strain maintains a low plasma insulin level, which may account in part why certain loci from NON/ShiLt can enhance development of autoimmune type 1 diabetes in segregating hybrid mice following outcross to NOD/ShiLtJ. The NON strain-characteristic immunologic abnormalities include perivascular/periductular leukocyte infiltration into the pancreas and submandibular salivary glands, and T lymphocytopenia evident by 20 weeks of age in spleen. NON/ShiLt mice clearly harbor genes predisposing to type 2 diabetes, as evidenced by early impaired glucose tolerance in males and females, development of moderate mature-onset obesity in the presence of low plasma insulin levels, and development of glomerulosclerotic kidney lesions. The ALS/Lt strain shares the H2nb1 MHC haplotype with NON/ShiLt. Although ALS/Lt males share the impaired glucose tolerance phenotype of NON/ShiLt males, the ALS/Lt males differ in developing progressive hyperinsulinemia as they gain weight whereas NON/ShiLt males fail to hypersecrete insulin, suggesting a potential beta cell response defect in the latter strain. F1 hybrids of NON/ShiLt and NZO/Hl provide a new model of obesity-induced diabetes. Male (NON/ShiLt x NZO/Hl)F1 hybrids are obese (Body Weight = 53.5 g by 16 wks) and almost all develop maturity onset NIDDM. F1 males on a 4% diet will develop hyperglycemia around 20 to 24 weeks of age; increasing the fat content of the diet accelerates diabetes onset to 16 to 20 wks of age. (NZO/Hl x NON/ShiLt)F1 hybrids will develop diabetes slightly faster than their reciprocal cross due to the NZO maternal environment; however this cross is difficult to produce due to the inherently poor breeding performance of NZO/HlJ female mice. F1 females exhibit a weight gain similar to the NZO parent, and have impaired glucose tolerance but are resistant to diabetes development. Diabetes development can be accelerated to 8-12 weeks by fostering onto an F1 dam. Reciprocal backcrosses to the parental strains and analysis of (NON/ShiLt x NZO/Hl)F2 mice has led to the identification of a number of complex diabetes-predisposing ("diabesity") QTLs. Dr. Leiter's research group at The Jackson Laboratory is currently developing a series of 9 recombinant congenic strains (RCS) made by backcrossing the (NZO/Hl x NON/ShiLt)F1 for two generations onto the NON/Lt background before inbreeding (~12% NZO/Hl, 88% NON/ShiLt genomes). Preliminary analysis indicates that body weight gains of all RCS are higher than NON/ShiLt, but none are as obese as NZO/Hl; some of these RCS develop NIDDM while others are resistant. These new strains will be useful to further analyze diabesity QTLs and as new models for type 2 (NIDDM) diabetes. An additional benefit of the RCS is better breeding performance than NZO/Hl.Strain Development
The NON inbred strain arose out of a colony originally developed by selection for high fasting blood glucose early in the inbreeding of the Cataract Shionogi (CTS) strain. These mice were originally outbred Jcl:ICR mice. A cataract-free substrain was initiated at F6, with selection made on the basis of a high fasting blood glucose. This line was separated from the future NOD/Shi line at F13, and originally designated NON for nonobese nondiabetic.
Gene & Allele Details
| 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; | ||
| General Note |
Pde6brd1, retinal degeneration 1, recessive. Formerly r, rd, rd1. A mutation causing retinal degeneration described by Bruckner (J:25576) and by Tansley (J:15333) in various stocks was later found to be present in many inbred strains (J:114). Keeler (J:5007) thought it to be identical with the rodless retina mutation he had described in 1924 (J:24999); the identity has recently been proven by analyses of DNA from Keeler's original slides (J:15231). Homozygotes are fully viable and fertile.Eyes develop normally up to 7 to 10 days after birth. At this stage the outer segment of the rod cell has begun to form, and in wild type mice it elongates rapidly during the 10th to 15th days. In Pde6brd1/Pde6brd1 mice the nascent outer segments and the rod cells degenerate rapidly so that by 15 days there is only a thin layer of rod cells left, and they have disappeared completely by 35 days (J:5250, J:5708). The inner nuclear layer and the retinal ganglion cells appear normal butmay show slight quantitative reduction (J:5812, J:5292). Although the eyes of Pde6brd1 homozygotes are devoid of normal rods, the mice have some visual capacity (J:5980). About 3% of cones among the visual cells degenerate at a much slower rate than do rods, so that a few cones are still present at 18 months (J:5988). The surviving cones are postulated (J:25157) as the light receptors required for the persistence of circadian responses to dawn and dusk in Pde6brd1 homozygotes past the sstage when rods have disappeared (J:29236). In fusion chimeras between wild type and Pde6brd1 homozygous embryos, the Pde6brd1 mutant acts in the photoreceptor cells rather than in the pigment epithelium of the retina (J:5708). Action within photoreceptor cells is also implied by the long term survival of wild type rod cells transplanted into Pde6brd1 homozygote retinas (J:20769). At a stage before degeneration can be seen, a deficiency of cGMP-PDE, andan excess of cGMP, appears in rod photoreceptor cells (J:5332). The rate of retinal degeneration in mutants doubly homozygous for two retinal degeneration mutations (Pde6brd1 and RdsRd2) is intermediate between those of the two homozygotes (J:12044). The double homozygote shows an intermediate level of mRNAs for the ß subunit of cGMP-PDE and for several other phototransduction related proteins, suggesting an interaction between Pde6brd1 and RdsRd2 (J:2579). Genbank ID for mutant sequence: M75166 | ||
| 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
Strains carrying Pde6brd1 allele
View Strains carrying Pde6brd1 (74 strains)
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: NON
Additional Web Information
Genetic Quality Control Annual Report
JAX Notes, Fall 2002; 487. New Polygenic Obesity Mouse Models.
JAX Notes, Fall 2006; 503. NON/LtJ Males: a New Model of Diet-induced Diabesity.
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 AX11
Room Number MP19
Research Applications
This mouse can be used to support research in many areas including:
Pde6brd1 relatedDiabetes and Obesity Research
Obesity Without Diabetes (moderate, adult onset)
Type 1 Diabetes (IDDM) Analysis Strains (Related Inbred Strains)
Type 2 Diabetes (NIDDM) (pre-type 2)
Immunology and Inflammation Research
Autoimmunity
Sensorineural Research
Retinal Degeneration (Homozygous for Pde6brd1)
Mouse/Human Gene Homologs
retinitis pigmentosa, autosomal recessive
Sensorineural Research
Retinal Degeneration
References
Selected Reference(s)
Additional ReferencesGraser RT; Mathews CE; Leiter EH; Serreze DV. 1999. MHC characterization of ALR and ALS mice: respective similarities to the NOD and NON strains. Immunogenetics 49(7-8):722-6. [PubMed: 10369935] [MGI Ref ID J:56048]
Leiter EH; Reifsnyder PC; Flurkey K; Partke HJ; Junger E; Herberg L. 1998. NIDDM genes in mice: deleterious synergism by both parental genomes contributes to diabetogenic thresholds. Diabetes 47(8):1287-95. [PubMed: 9703330] [MGI Ref ID J:48957]
Makino S; Kunimoto K; Muraoka Y; Mizushima Y; Katagiri K; Tochino Y. 1980. Breeding of a non-obese, diabetic strain of mice. Jikken Dobutsu 29(1):1-13. [PubMed: 6995140] [MGI Ref ID J:25411]
Prochazka M; Leiter EH; Serreze DV; Coleman DL. 1987. Three recessive loci required for insulin-dependent diabetes in nonobese diabetic mice [published erratum appears in Science 1988 Nov 11;242(4880):945] Science 237(4812):286-9. [PubMed: 2885918] [MGI Ref ID J:8783]
Prochazka M; Serreze DV; Worthen SM; Leiter EH. 1989. Genetic control of diabetogenesis in NOD/Lt mice. Development and analysis of congenic stocks. Diabetes 38(11):1446-55. [PubMed: 2576007] [MGI Ref ID J:29464]
Reifsnyder PC; Churchill G; Leiter EH. 2000. Maternal environment and genotype interact to establish diabesity in mice. Genome Res 10(10):1568-78. [PubMed: 11042154] [MGI Ref ID J:65256]
Price and Supply Information
| Strain Name: | NON/ShiLtJ |
| Stock Number: | 002423 |
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 | Repository-Live. A collection of over 1000 strains maintained as live colonies. Individual colonies are sized to meet current customer demand. Delivery for orders of 10 mice or less ranges on average from one to eight weeks; mice are generally shipped between four to six weeks of age with a maximum shipping age of ~nine weeks. Colony sizes do not generally support stringent age specifications for large volumes of mice; however custom orders and larger quantities of mice are easily arranged. Estimated ship dates for all orders provided within 48 hours of order placement. |
|---|---|
| Supply Notes |
This strain is also kept on a 10% fat diet to be used as controls for NONcNZO10/LtJ (004456). To order from this colony, request stock number 302423. Usually shipped between four and six weeks of age. This strain is included in the Mouse Mutant Resource collection. 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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