Type 1 diabetes and the control of dexamethazone-induced apoptosis in mice maps to the same region on chromosome 6

Genomics. 1995 Aug 10;28(3):398-404. doi: 10.1006/geno.1995.1167.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / drug effects
  • Apoptosis / genetics*
  • Cells, Cultured
  • Chromosome Mapping*
  • Dexamethasone / pharmacology*
  • Diabetes Mellitus, Type 1 / genetics*
  • Drug Resistance
  • Female
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Inbred NOD
  • Phenotype
  • Thymus Gland / cytology

Substances

  • Dexamethasone