| |||||||
- Description
- Phenotype
- Genes & alleles
- Genotyping
- Health & husbandry
- References
- Purchasing information
- Terms of Use
Description
Strain Information
Former Names c6 c17 (Changed: 15-DEC-04 ) Type Congenic; Mutant Strain; Additional information on Genetically Engineered Mutant Mice. Species laboratory mouse Background Strain C57BL/6 Donor Strain NOD/Uf H2 Haplotype b Generation NE7F?+14p (08-JAN-04) Donating Investigator Wakeland, Appearance
black
Related Genotype: a/aDescription
This strain is doubly congenic for a 19 cM segment of Chr 17 (called c17 in Yui et al.) extending from D17Mit21through D17Mit10and including the major histocompatibility complex, H2,and the insulin dependent diabetes susceptibility locus Idd1and for a 24 cM segment (called c6 by Yui et al.)of Chr 6 extending from D6Mit54through D6Mit14and including the insulin dependent diabetes susceptibility locus Idd6.No information has been published for this double congenic strain. However, upon histologic examination of the pancreas, a significantly higher percentage of B6.NOD-(D17Mit21-D17Mit10) singly congenic mice than of C57BL/6J control mice were found to exhibit periinsulitis, and more extensive mononuclear cell infiltrates were observed in the pancreata of these mice. The pancreatic infiltrates were not associated specifically with the islets. Insulitis (intraislet infiltration) was extremely rare, and no more than one affected islet was observed in a single animal, even in cases where extensive perivascular/periductal infiltrates existed. Incidence and severity of periinsulitis in B6.NOD-(D6Mit54-D6Mit14) mice were similar to those of controls. Male and female B6.NOD-(D17Mit21-D17Mit10) mice exhibited similar incidence of pancreatic infiltration; female NOD mice are more susceptible than males to both insulitis and diabetes.Development
Genomic segments found in earlier linkage studies to include diabetogenic loci were transferred in the laboratory of E.K. Wakeland from NOD/Uf to C57BL/6 by six successive backcrosses (to N7). Sibs of each lineage were then intercrossed to generate mice homozygous for each segment. Microsatellite analysis was used to type mice for loci in the regions of interest. The B6.NOD-(D6Mit54-D6Mit14) (D17Mit21-D17Mit10) double congenic strain was created by crossing mice of the singly congenic B6.NOD-(D17Mit21-D17Mit10) and B6.NOD-(D6Mit54-D6Mit14) strains, then breeding to homozygosity for both congenic segments.
Control Information
| Control | ||
|---|---|---|
| 000664 C57BL/6J | ||
| Considerations for Choosing Controls | ||
Related Strains
Strains carrying H2g7 allele
View Strains carrying H2g7 (9 strains)
003063 B6.NOD-(D6Mit54-D6Mit14)/J
Additional Web Information
Congenic Nomenclature
Phenotype
Phenotype Information
This mouse can be used to support research in many areas including:
H2g7 relatedImmunology and Inflammation Research
Inflammation
Idd6NOD relatedImmunology and Inflammation Research
CD Antigens, Antigen Receptors, and Histocompatibility Markers
Diabetes and Obesity Research
Type 1 Diabetes (IDDM) Analysis Strains (NOD/ShiLtJ MHC Congenics)
Immunology and Inflammation Research
Autoimmunity
CD Antigens, Antigen Receptors, and Histocompatibility Markers
Genes & Alleles
Gene & Allele Information
| Gene Symbol and Name | D17Mit10, DNA segment, Chr 17, Massachusetts Institute of Technology 10 | ||
|---|---|---|---|
| Chromosome | 17 | ||
| Gene Symbol and Name | D17Mit21, DNA segment, Chr 17, Massachusetts Institute of Technology 21 | ||
| Chromosome | 17 | ||
| Gene Symbol and Name | D6Mit54, DNA segment, Chr 6, Massachusetts Institute of Technology 54 | ||
| Chromosome | 6 | ||
| Gene Symbol and Name | D6Mit14, DNA segment, Chr 6, Massachusetts Institute of Technology 14 | ||
| Chromosome | 6 | ||
| Allele Symbol | H2g7 | ||
| Allele Name | g7 variant | ||
| Allele Type | Not Applicable | ||
| Gene Symbol and Name | H2, histocompatibility-2, MHC | ||
| Chromosome | 17 | ||
| Gene Common Name(s) | H-2; MHC-II; | ||
| Allele Symbol | Idd1NOD/Uf | ||
| Allele Name | NOD/Uf | ||
| Allele Type | QTL | ||
| Strain of Origin | NOD/Uf | ||
| Gene Symbol and Name | Idd1, insulin dependent diabetes susceptibility 1 | ||
| Chromosome | 17 | ||
| Gene Common Name(s) | Idd-1; | ||
| General Note |
NOD is homozygous for recessive alleles for susceptibility at all three loci, Idd1s, Idd2s, and Idd3s. The dominant alleles for non-susceptibility to IDD, Idd1r, etc., occur in the NON strain. Homozygosity for the recessive alleles at all three loci is necessary for the development of IDD.The Idd1 locus is linked to the major histocompatibility locus on Chr 17, but Idd2 is on Chr 9 (1) and Idd3 is on Chr 3 (J:8783, J:3351). This locus is also linked to peripheral CD4 lymphocytosis. | ||
| Molecular Note | This allele confers increased periinsulitis and increased CD4 lymphocytosis compared to C57BL/6. [MGI Ref ID J:33172] | ||
| Allele Symbol | Idd6NOD | ||
| Allele Name | NOD | ||
| Allele Type | QTL | ||
| Strain of Origin | NOD | ||
| Gene Symbol and Name | Idd6, insulin dependent diabetes susceptibility 6 | ||
| Chromosome | 6 | ||
| Gene Common Name(s) | Idd-6; | ||
| General Note | This allele also confers defective IFN-gamma response in NK cells on a C57BL/6 genetic background (J:85823). | ||
| Molecular Note | This allele confers impaired thymocyte proliferation compared to C57BL/6. [MGI Ref ID J:72360] | ||
Genotyping
Genotyping Information
This strain will not have a genotyping protocol or one is not currently available.
Helpful Links
Optimizing PCR Protocols
References
References
Additional References
Rogner UC; Boitard C; Morin J; Melanitou E; Avner P. 2001. Three loci on mouse chromosome 6 influence onset and final incidence of type i diabetes in nod.c3h congenic strains. Genomics 74(2):163-71. [PubMed: 11386752] [MGI Ref ID J:69992]
Yui MA; Muralidharan K; Moreno-Altamirano B; Perrin G; Chestnut K; Wakeland EK. 1996. Production of congenic mouse strains carrying NOD-derived diabetogenic genetic intervals: an approach for the genetic dissection of complex traits. Mamm Genome 7(5):331-4. [PubMed: 8661724] [MGI Ref ID J:33172]
H2g7 relatedIdd1NOD/Uf relatedCarrasco-Marin E; Shimizu J; Kanagawa O; Unanue ER. 1996. The class II MHC I-Ag7 molecules from non-obese diabetic mice are poor peptide binders. J Immunol 156(2):450-8. [PubMed: 8543793] [MGI Ref ID J:30538]
Fossati G; Cooke A; Papafio RQ; Haskins K; Stockinger B. 1999. Triggering a second T cell receptor on diabetogenic T cells can prevent induction of diabetes. J Exp Med 190(4):577-83. [PubMed: 10449528] [MGI Ref ID J:108724]
Gray D; Abramson J; Benoist C; Mathis D. 2007. Proliferative arrest and rapid turnover of thymic epithelial cells expressing Aire. J Exp Med 204(11):2521-8. [PubMed: 17908938] [MGI Ref ID J:126040]
Jasinski JM; Yu L; Nakayama M; Li MM; Lipes MA; Eisenbarth GS; Liu E. 2006. Transgenic insulin (B:9-23) T-cell receptor mice develop autoimmune diabetes dependent upon RAG genotype, H-2g7 homozygosity, and insulin 2 gene knockout. Diabetes 55(7):1978-84. [PubMed: 16804066] [MGI Ref ID J:111874]
Klein J; Figueroa F; David CS. 1983. H-2 haplotypes, genes and antigens: second listing. II. The H-2 complex. Immunogenetics 17(6):553-96. [PubMed: 6407984] [MGI Ref ID J:7097]
Leiter EH. 1998. NOD Mice and Related Strains: Origins, Husbandry and Biology Introduction. In: NOD Mice and Related Strains: Research Applications in Diabetes, AIDS, Cancer, and Other Diseases. RG Landes, Austin. [MGI Ref ID J:110093]
Levisetti MG; Lewis DM; Suri A; Unanue ER. 2008. Weak proinsulin peptide-major histocompatibility complexes are targeted in autoimmune diabetes in mice. Diabetes 57(7):1852-60. [PubMed: 18398138] [MGI Ref ID J:138230]
Luhder F; Katz J; Benoist C; Mathis D. 1998. Major histocompatibility complex class II molecules can protect from diabetes by positively selecting T cells with additional specificities. J Exp Med 187(3):379-87. [PubMed: 9449718] [MGI Ref ID J:108722]
Mahler M; Bristol IJ; Leiter EH; Workman AE; Birkenmeier EH; Elson CO; Sundberg JP. 1998. Differential susceptibility of inbred mouse strains to dextran sulfate sodium-induced colitis. Am J Physiol 274(3 Pt 1):G544-51. [PubMed: 9530156] [MGI Ref ID J:46553]
Martin-Orozco N; Chen Z; Poirot L; Hyatt E; Chen A; Kanagawa O; Sharpe A; Mathis D; Benoist C. 2003. Paradoxical dampening of anti-islet self-reactivity but promotion of diabetes by OX40 ligand. J Immunol 171(12):6954-60. [PubMed: 14662903] [MGI Ref ID J:86926]
Pearson T; Markees TG; Serreze DV; Pierce MA; Marron MP; Wicker LS; Peterson LB; Shultz LD; Mordes JP; Rossini AA; Greiner DL. 2003. Genetic disassociation of autoimmunity and resistance to costimulation blockade-induced transplantation tolerance in nonobese diabetic mice. J Immunol 171(1):185-95. [PubMed: 12816997] [MGI Ref ID J:109845]
Podolin PL; Pressey A; DeLarato NH; Fischer PA; Peterson LB; Wicker LS. 1993. I-E+ nonobese diabetic mice develop insulitis and diabetes. J Exp Med 178(3):793-803. [PubMed: 8350054] [MGI Ref ID J:14178]
Serreze DV; Gallichan WS; Snider DP; Croitoru K; Rosenthal KL; Leiter EH; Christianson GJ; Dudley ME; Roopenian DC. 1996. MHC class I-mediated antigen presentation and induction of CD8+ cytotoxic T-cell responses in autoimmune diabetes-prone NOD mice. Diabetes 45(7):902-8. [PubMed: 8666141] [MGI Ref ID J:33688]
Turley SJ; Lee JW; Dutton-Swain N; Mathis D; Benoist C. 2005. Endocrine self and gut non-self intersect in the pancreatic lymph nodes. Proc Natl Acad Sci U S A 102(49):17729-33. [PubMed: 16317068] [MGI Ref ID J:104385]
Wong FS; Du W; Thomas IJ; Wen L. 2005. The influence of the major histocompatibility complex on development of autoimmune diabetes in RIP-B7.1 mice. Diabetes 54(7):2032-40. [PubMed: 15983204] [MGI Ref ID J:109830]
Yoshida T; Jiang F; Honjo T; Okazaki T. 2008. PD-1 deficiency reveals various tissue-specific autoimmunity by H-2b and dose-dependent requirement of H-2g7 for diabetes in NOD mice. Proc Natl Acad Sci U S A 105(9):3533-8. [PubMed: 18299579] [MGI Ref ID J:132764]
Zhang C; Todorov I; Lin CL; Atkinson M; Kandeel F; Forman S; Zeng D. 2007. Elimination of insulitis and augmentation of islet beta cell regeneration via induction of chimerism in overtly diabetic NOD mice. Proc Natl Acad Sci U S A 104(7):2337-42. [PubMed: 17267595] [MGI Ref ID J:119749]
Idd6NOD relatedKoarada S; Wu Y; Yim YS; Wakeland EW; Ridgway WM. 2004. Nonobese diabetic CD4 lymphocytosis maps outside the MHC locus on chromosome 17. Immunogenetics 56(5):333-7. [PubMed: 15309345] [MGI Ref ID J:92304]
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]
Todd JA; Aitman TJ; Cornall RJ; Ghosh S; Hall JR; Hearne CM; Knight AM; Love JM; McAleer MA; Prins JB; Rodrigues N; Lathrop M; Pressey A; DeLarato NH; Peterson LB; Wicker LS. 1991. Genetic analysis of autoimmune type 1 diabetes mellitus in mice [see comments] Nature 351(6327):542-7. [PubMed: 1675432] [MGI Ref ID J:3351]
Yui MA; Muralidharan K; Moreno-Altamirano B; Perrin G; Chestnut K; Wakeland EK. 1996. Production of congenic mouse strains carrying NOD-derived diabetogenic genetic intervals: an approach for the genetic dissection of complex traits. Mamm Genome 7(5):331-4. [PubMed: 8661724] [MGI Ref ID J:33172]
Bergman ML; Duarte N; Campino S; Lundholm M; Motta V; Lejon K; Penha-Goncalves C; Holmberg D. 2003. Diabetes protection and restoration of thymocyte apoptosis in NOD Idd6 congenic strains. Diabetes 52(7):1677-82. [PubMed: 12829632] [MGI Ref ID J:84296]
Bergman ML; Penha-Goncalves C; Lejon K; Holmberg D. 2001. Low rate of proliferation in immature thymocytes of the non-obese diabetic mouse maps to the Idd6 diabetes susceptibility region. Diabetologia 44(8):1054-61. [PubMed: 11484085] [MGI Ref ID J:72360]
Matsuki N; Stanic AK; Embers ME; Van Kaer L; Morel L; Joyce S. 2003. Genetic dissection of V alpha 14J alpha 18 natural T cell number and function in autoimmune-prone mice. J Immunol 170(11):5429-37. [PubMed: 12759418] [MGI Ref ID J:85823]
Vallois D; Gagnerault MC; Avner P; Rogner UC; Boitard C; Benlagha K; Herbelin A; Lepault F. 2008. Influence of a non-NK complex region of chromosome 6 on CD4+ invariant NK T cell homeostasis. J Immunol 181(3):1753-9. [PubMed: 18641312] [MGI Ref ID J:137837]
Health & husbandry
Health & Colony Maintenance Information
Currently there no information available for this strain. This may be due to the supply level of this strain.
Purchasing information
Pricing, Supply Level & Notes, Controls, General Terms & Conditions
Pricing
| Pricing for USA, Canada and Mexico shipping destinations |
|
*Price(s) in US dollars ($)
Weeks of Age Price* Gender Cryorecovery Fee $1900.00
Additional Supply Details
| Pricing for International shipping destinations |
|
*Price(s) in US dollars ($)
Weeks of Age Price* Gender Cryorecovery Fee $2470.00
Additional Supply Details
|
|
|
Supply Details
| Standard Supply | Repository-Cryopreserved. Must Be Recovered. Please refer to pricing and supply notes for further information. |
|---|---|
| Supply Notes |
|
Control Information
| Control | ||
|---|---|---|
| 000664 C57BL/6J | ||
| Considerations for Choosing Controls | ||
| USA, Canada and Mexico - Control Pricing Information for Genetically Engineered Mutant Strains. | ||
| International - Control Pricing Information for Genetically Engineered Mutant Strains. | ||
General Terms and Conditions
See Terms of Use
The Jackson Laboratory's Genotype Promise
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
Purchasing Information
JAX® Mice Orders
Surgical Services
Contact Information
Orders & Technical Support
Tel: 800.422.6423 or 207.288.5845
Fax: 207.288.6150
Technical Support Email Form
Terms of Use
Terms of Use
General Terms and Conditions
Contact information
General inquiries
Contracts Administration
| phone: | 207-288-6470 |
| fax: | 207-288-6655 |
JAX® Mice & Services Conditions of Use
“Each recipient institution, including its employees and other researchers under its control (RECIPIENT), of mice or services using mice from The Jackson Laboratory (TJL) agrees that such mice, descendants of those mice derived by inbreeding or crossbreeding, including unmodified derivatives of those mice or their descendants (“MICE”) shall not be: (i) used for any purpose other than the internal research of the RECIPIENT, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services with respect to MICE. Acceptance of MICE from TJL shall be deemed agreement by RECIPIENT to these conditions, and departure from these conditions requires The Jackson Laboratory’s prior written authorization.”No Warranty
MICE, PRODUCTS AND SERVICES ARE PROVIDED “AS IS”. THE LABORATORY EXTENDS NO WARRANTIES OF ANY KIND, EITHER EXPRESS, IMPLIED, OR STATUTORY, WITH RESPECT TO MICE, PRODUCTS OR SERVICES, INCLUDING ANY IMPLIED WARRANTY OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE, OR ANY WARRANTY OF NON-INFRINGEMENT OF ANY PATENT, TRADEMARK, OR OTHER INTELLECTUAL PROPERTY RIGHTS.
In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of MICE, products or services, The Jackson Laboratory will, at its option, provide credit or replacement for the MICE or product received or the services provided.
No Liability
In no event shall The Jackson Laboratory, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, products or services, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of The Jackson Laboratory, its agents or employees. In purchasing or receiving MICE, products or services from The Jackson Laboratory, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges The Jackson Laboratory from all such causes of action or damages, and further agrees to defend and indemnify The Jackson Laboratory from any costs or damages arising out of any third party claims.
MICE and biological materials are to be used in a safe manner and in accordance with all applicable governmental rules and regulations.
The foregoing represents the General Terms and Conditions applicable to The Jackson Laboratory’s MICE, products and services. In addition, special terms and conditions of sale of certain MICE, products and services may be set forth separately in The Jackson Laboratory web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, products and services by The Jackson Laboratory, and by its licensees and distributors.
Acceptance of delivery of MICE, products or services shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on The Jackson Laboratory, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, products services by The Jackson Laboratory.