Mapping Data

Experiment

• Experiment
  TEXT-QTL
• Chromosome
  8
• Reference
  J:86633 Mathews CE, et al., Genetic analysis of resistance to Type-1 Diabetes in ALR/Lt mice, a NOD-related strain with defenses against autoimmune-mediated diabetogenic stress. Immunogenetics. 2003 Oct;55(7):491-6
• ID
  MGI:2683520

Genes

Gene	Assay Type
D8Mit80	PCR amplified length variant
Idd22	resistance/susceptibility

Notes

• Experiment
  120 (NOD/Lt x ALR/Lt) x NOD/Lt backcross animals were genotyped at 88 loci with an average resolution of 20 cM to identify QTLs associated with reactive oxygen species-induced diabetes via pancreatic islet cell damage. Parental strain NOD/Lt is susceptible to free radical-induced diabetes whereas parental strain ALR/Lt is resistant to free radical-induced diabetes.
  
  Idd16 on mouse Chromosome 17 was detected in this study with LOD=4.1 near D17Mit16. Idd16 maps at 17.4 cM near the H2 locus. The QTL interval of Idd16 spans 16 cM to 20 cM. This locus appears to interact with another locus on mouse Chromosome 8 named Idd21.
  
  A novel locus named Idd22 mapped to 41 cM on mouse Chromosome 8 with LOD=4.4 at D8Mit80. The QTL interval of Idd22 spans 36 cM to 55 cM.ALR/Lt-derived alleles confer dominantly inherited resistance to diabetes at Idd21. Idd21 appears to interact with Idd16. Animals homozygous for NOD/Lt-derived alleles at both Idd16 and Idd22 exhibit significantly increased diabetes incidence.
  
  A suggestive locus mapped to 33 cM on mouse Chromosome 3 with LOD=2.4 at D3Mit241. This locus spans 20 cM to 50 cM and overlaps with a previously mapped QTL named Susp (suppressor of superoxide production). ALR/Lt-derived alleles confer resistance to diabetes at this locus.