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Description
Strain Information
Former Names NOD/LtSz-Prkdcscid Tg(Ins2-GAD2)2Lt/LtJ (Changed: 01-DEC-05 ) NOD.Cg-Prkdcscid Tg(GAD2)2Lt/Lt (Changed: 28-NOV-05 ) NOD.Cg-Prkdcscid Tg(GAD2)2Lt (Changed: 23-NOV-05 ) NOD/Lt-Prkdcscid Tg(GAD2)2Lt (Changed: 15-DEC-04 ) Type Coisogenic; Congenic; Mutant Strain; Spontaneous Mutation; Transgenic; Additional information on Genetically Engineered Mutant Mice. Species laboratory mouse H2 Haplotype g7 Generation N2F31p (29-JAN-06) Donating Investigator Edward Leiter, The Jackson Laboratory Appearance
albino, pink eyed
Related Genotype: A/A Tyrc/TyrcDescription
NOD.Cg-Prkdcscid Tg(Ins2-GAD2)2Lt/LtJ transgenic mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Transgenic mice are homozygous for Prkdcscid and are free of potential insulitic lymphocytes resulting in diabetes resistance. Delayed diabetes onset is observed when splenic lymphocytes from 5 week old pre-diabetic NOD females are adoptively transferred into NOD transgenic mice homozygote for Prkdcscid when compared to adoptive transfers into control NOD females. Similar to the NOD/ShiLt(Cg)-Tg(Ins2-GAD2)2Lt/J (Stock No. 005870) homozygous transgenic mice are developmentally lethal due to the transgene insertion site (Bridgett et al, Diabetes 1998 47:1848-56).This model provides a tool for studying the role of GAD2 as an islet autoantigen in the NOD mouse model of Type 1 diabetes.
Development
The transgene Ins2-GAD2 encodes the human glutamic acid decarboxylase2 cDNA under the control of the rat insulin 2 promoter. This transgenic construct was injected into NOD/Lt oocytes and the resulting founders were backcrossed to wildtype siblings. NOD transgenic mice were backcrossed 1 generation to NOD.CB17-Prkdcscid prior to intercrossing to make homozygote for the Prkdcscid mutation (Bridgett et al, Diabetes 1998 47:1848-56). In 2005, the Type 1 Diabetes Resource received NOD/LtSz-Prkdcscid Tg(Ins2-GAD2)2Lt/LtJ at generation N2F31.
Control Information
| Control | ||
|---|---|---|
| Noncarrier | ||
| 003073 NOD/Lt-Tg(GAD2)2Lt | ||
| Considerations for Choosing Controls | ||
Related Strains
Strains carrying Prkdcscid allele
View Strains carrying Prkdcscid (25 strains)
005870 NOD/ShiLt(Cg)-Tg(Ins2-GAD2)2Lt/J
003843 NOD.Cg-Prkdcscid Tg(Ins2-GAD2)1Lt/LtJ 003074 NOD/ShiLt-Tg(Ins2-GAD2)1Lt/LtJ
Additional Web Information
Congenic Nomenclature
Phenotype
Phenotype Information
This mouse can be used to support research in many areas including:
Prkdcscid relatedResearch Tools
Immunology and Inflammation Research (B and T cell deficiency)
Immunology and Inflammation Research
Immunodeficiency (B and T cell deficiency)
Internal/Organ Research
Lymphoid Tissue Defects (B and T cell deficiency)
Research Tools
Cancer Research (B and T cell deficiency) (xenograft/transplant host)
Toxicology Research (xenograft/transplant host)
Virology Research
B and T Cell Deficiency (AIDS research tool)
Genes & Alleles
Gene & Allele Information
| Allele Symbol | Prkdcscid | ||
|---|---|---|---|
| Allele Name | severe combined immunodeficiency | ||
| Allele Type | Spontaneous | ||
| Common Name(s) | scid; | ||
| Strain of Origin | CB17 | ||
| Gene Symbol and Name | Prkdc, protein kinase, DNA activated, catalytic polypeptide | ||
| Chromosome | 16 | ||
| Gene Common Name(s) | AI326420; AU019811; DNA-PK; DNA-PKcs; DNAPDcs; DNAPK; DNPK1; HYRC; HYRC1; MGC189093; XRCC7; expressed sequence AI326420; expressed sequence AU019811; p350; scid; severe combined immunodeficiency; slip; | ||
| General Note |
The Prkdcscid mutation arose in the C.B-17 inbred strain (BALB/c.C57BL/Ka-Igh-1b) (J:9341). Most homozygotes have no detectable IgM, IgG1, IgG2a, IgG2b, IgG3, or IgA, but a few have low levels of one to three of these immunoglobulin isotypes. The size of the lymphoid organs is only one-tenth or less that of normal. Thymus, lymph nodes, and splenic follicles are virtually devoid of lymphocytes (J:30980). Homozygotes are deficient in both B and T cell function. Their spleen cells do not respond to either B or T cell mitogens and they are unable to reject skin grafts. They lack detectable B cells and pre-B cells. In spite of the small thymus and lack of functional T cells, the Thy1 marker is present on a majority of cells recovered from the thymus, and T cell lymphomas occur in 10 per cent or more of affected mice. Prkdcscid specifically impairs differentiation of stem cells into mature lymphocytes. Myeloid cell differentiation is not affected. The basic defect in these mice appears to be in the lymphoid stem cells and not in the cellular environment, since functional T and B cells are found in mice reconstituted with normal bone marrow (J:30980, J:7343). However, full reconstitution of the immune deficiency occurs only after irradiation of the recipients, indicating that Prkdcscid/Prkdcscid mice may have normal numbers of a radiation-sensitive stem cell that has defective proliferative capacity (J:8299). The rearrangements of immunoglobulin and T cell receptor genes that normally occur in B and T lymphocytes are not found in homozygous Prkdcscid mice. However, in Abelson leukemia virus-transformed B cells of these mice and in their occasional T cell lymphomas, rearrangements, most of which are abnormal, are found. This suggests that scid may act through an effect on the recombinase system catalyzing the assembly of immunoglobulin and T cell receptor genes, and that lymphocytes with these defects are not able to develop further (J:8420). Although most Prkdcscid homozygotes fail to produce immunoglobulin and functional T-cell receptor, some produce these products at low levels, with an occasional mouse with nearly normal levels of serum immunoglobulin, the criterion usually used tomeasure the effects of Prkdcscid. This phenomenon is referred to as "leakiness" of the VDJ recombination defect (J:4610).Homozygous Prkdcscidmice are fertile and, under specific pathogen-free conditions, may survive a year or more(J:6958). The Prkdcscid mouse has been widely used in studies of the immune system, in particular of VDJ recombination in T and B lymphocytes. Its lack of immunocompetence has made it useful in transplantation studies, particularly transplantation and development of metastasis in human tumors. The interaction of infection, immunity, and disease processes have been studied with these mice. Poole (J:31292) offers a brief review of the nature and usefulness of the Prkdcscid mouse, with key references to the very extensive literature. Mutant mRNA does not appear to differ from wild-type although protein expression is reduced more than 10-fold. Mutant protein is defective for nuclear association but exhibits normal DNA-binding ability. NOD.Cg-Prkdcscid B2mtm1Unc mice lack mature lymphocytes and serum Ig, are MHC class I deficient, B and T cell deficient, C-5 deficient (Hc0), and have low NK cells. These mice display accumulation of iron in the liver and rapid clearance of human IgG1. | ||
| Molecular Note | A T-to-A transversion point mutation at a position corresponding to codon 4095 created a premature stop codon. [MGI Ref ID J:35393] [MGI Ref ID J:39329] | ||
| Allele Symbol | Tg(Ins2-GAD2)2Lt | ||
| Allele Name | transgene insertion 2, Edward H Leiter | ||
| Allele Type | Transgenic (random, expressed) | ||
| Common Name(s) | TgN(RIP7hGAD65)Lt4 (A line); TgN(RIP7hGAD65)Lt4 A-line; | ||
| Mutation Made By | Edward Leiter, The Jackson Laboratory | ||
| Strain of Origin | NOD/ShiLt | ||
| Expressed Gene | GAD2, glutamate decarboxylase 2 (pancreatic islets and brain, 65kDa), human | ||
| Promoter | Ins2, insulin 2, rat | ||
| Molecular Note | The transgene comprises the cDNA sequence encoding human glutamic acid decarboxylase 2 under control of a modified rat insulin 2 promoter composed of 9.5 kb of genomic DNA from upstream of the transcription initiation site fused to the first intron of Ins2. Densitrometric Southern blot analysis indicates presence of 4-5 copies of the transgene. FISH analysis and pseudo-Giemsa metaphase spread analysis showed integration to have occurred near the centromere of Chr 15. Expression in the pancreatic islets of transgenic mRNA has been demonstrated by reverse transcription followed by PCR (RT-PCR), and of GAD2 protein by western blot analysis. [MGI Ref ID J:100251] | ||
Genotyping
Genotyping Information
Genotyping Protocols
Prkdcscid, PYRO, vers. 2
Prkdcscid, REST, vers. 1
Tg(Ins2-GAD2), STD PCR, vers. 1
Helpful Links
Optimizing PCR Protocols
References
References
Selected Reference(s)
Bridgett M; Cetkovic-Cvrlje M; O'Rourke R; Shi Y; Narayanswami S; Lambert J; Ramiya V; Baekkeskov S; Leiter EH. 1998. Differential protection in two transgenic lines of NOD/Lt mice hyperexpressing the autoantigen GAD65 in pancreatic beta-cells. Diabetes 47(12):1848-56. [PubMed: 9836515] [MGI Ref ID J:100251]
Additional References
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