Mapping Data

Experiment

• Experiment
  TEXT
• Chromosome
  4
• Reference
  J:63670 Lyons PA, et al., The NOD Idd9 genetic interval influences the pathogenicity of insulitis and contains molecular variants of Cd30, Tnfr2, and Cd137. Immunity. 2000 Jul;13(1):107-15
• ID
  MGI:1890107

Genes

Gene	Assay Type
Idd9	resistance/susceptibility
Idd9.1	resistance/susceptibility
Idd9.2	resistance/susceptibility
Idd9.3	resistance/susceptibility
D4Mit27	PCR amplified length variant
D4Mit59	PCR amplified length variant
D4Mit251	PCR amplified length variant
D4Mit226	PCR amplified length variant
D4Mit42	PCR amplified length variant
D4Mit127	PCR amplified length variant
Tnfrsf8	reported elsewhere
Tnfrsf1b	reported elsewhere
Tnfrsf9	reported elsewhere

Notes

• Experiment
  Two series of subcongenic lines derived from line NOD.B10 -Idd9 (NOD/MrkTacfBr and C57BL/10) were informative in mapping Idd9.1, Idd9.2 and Idd9.3 to mouse Chromosome 4. Idd9.1 was identified within a 35.7 congenic interval flanked by markers D4Mit27 andD4Mit59. Idd9.2 mapped to a 5.6 cM region flanked by D4Mit251 and D4Mit226. Idd9.3 mapped to a 2.0 cM region flanked by D4Mit127 and D4Mit42.
  
  The NOD.B10-Idd9 animals are highly resistant to development of diabetes but still exhibit mild to extensive insulitis.
  
  Candidate genes mapping within the Idd9.2 interval include Tnfrsf8 (formerly CD30) and Tnfrsf1b (formerly Tnfr2). Sequence analysis of Tnfrsf8 and Tnfrsf1b revealed amino acid differences between NOD/MrkTac and C57BL/10.
  
  Tnfrsf9 (formerly CD137)is a candidate gene mapping within the Idd9.3 interval. Sequence analysis of Tnfrsf9 revealed amino acid differences between NOD/MrkTac and C57BL/10.