Type 1 diabetes and the control of dexamethazone-induced apoptosis in mice maps to the same region on chromosome 6.
Quantitative trait loci mapping was used to identify the chromosomal location of genes that contribute to increase the resistance to apoptosis induced in immature CD4+8+ thymocytes. An F2 intercross of the nonobese diabetic (NOD) mouse (displaying an apoptosis-resistance phenotype) and the C57BL/6 mouse (displaying a nonresistance phenotype) was phenotypically analyzed and genotyped for 32 murine microsatellite polymorphisms. Maximum likelihood methods identified a region on the distal part of chromosome 6 that is linked to dexamethazone-induced apoptosis (lod score = 3.46) and accounts for 14% of the phenotypic variation. This chromosomal region contains the diabetes susceptibility locus Idd6, suggesting that the apoptosis-resistance phenotype constitutes a pathogenesis factor in IDDM of NOD mice.
D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000235:genetics*; D002478:Cells, Cultured; D002874:Chromosome Mapping; D003907:Dexamethasone / Q000494:pharmacology*; D003922:Diabetes Mellitus, Type 1 / Q000235:genetics*; D004351:Drug Resistance; D005260:Female; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D016688:Mice, Inbred NOD; D010641:Phenotype; D013950:Thymus Gland / Q000166:cytology
D003907:Dexamethasone