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Mapping Data
Experiment
  • Experiment
    TEXT-Congenic
  • Chromosome
    1
  • Reference
    J:88667 Hill NJ, et al., NOD Idd5 locus controls insulitis and diabetes and overlaps the orthologous CTLA4/IDDM12 and NRAMP1 loci in humans. Diabetes. 2000 Oct;49(10):1744-7
  • ID
    MGI:3036894
Genes
GeneAlleleAssay TypeDescription
Idd5 resistance/susceptibility
Idd5.1 resistance/susceptibility
D1Mit24 PCR amplified length variant
D1Mit303 PCR amplified length variant
Cflar reported elsewhere
Casp8 reported elsewhere
Cd28 reported elsewhere
Ctla4 reported elsewhere
Idd5.2 resistance/susceptibility
D1Mcg5 PCR amplified length variant
D1Mit46 PCR amplified length variant
D1Mit132 PCR amplified length variant
Slc11a1 reported elsewhere
Cxcr2 reported elsewhere
Notes
  • Experiment
    Idd5 on mouse Chromosome 1 was confirmed in a congenic strain carrying a C57BL/10J donor region spanning the entire Idd5 locus introgressed onto the NOD/MrkTac genetic background. Parental strain C57BL/10J is resistant to type 1 (insulin dependent diabetes) whereas parental strain NOD/MrkTac is susceptible. As expected, the congenic strain displayed resistance to type 1 diabetes.

    Refinement of the Idd5 locus was accomplished by creation of several subcongenic lines. Idd5 was resolved to 2 distinct loci,Idd5a at 33.8 cM and Idd5b at 41 cM on mouse Chromosome 1. Idd5a spans 32.8 cM (D1Mit124) - 34.8 cM (D1Mit303) and includes candidate genes Cflar, Casp8, Cd28, and Ctla4. Sequence analysis of Casp8 revealed several polymorphisms between C57BL/10J and NOD/MrkTac. Idd5b spans 39.3 cM (D1Mcg5) - 43.1 cM (D1Mit46/D1Mit132) and includes candidate genes Slc11a1 (Nramp1) and Il8rb (Cmkar2). A functional polymorphism exists in the Slc11a1 sequence between C57BL/10J and NOD/MrkTac. C57BL/10J-derived alleles conferresistance to type 1 diabetes at Nidd5a and Nidd5b.

    An interaction between Nidd5 and Nidd3 was also confirmed in this study. A double congenic carrying C57BL/10J donor DNA at both Nidd5 and Nidd3 on an NOD/MrkTac genetic background was constructed. Thedouble congenic is extremely resistant to both type 1 diabetes and insulitis.


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last database update
06/12/2024
MGI 6.13
The Jackson Laboratory