TYPE-1 DIABETES AND THE CONTROL OF DEXAMETHAZONE-INDUCED APOPTOSIS INMICE MAPS TO THE SAME REGION ON CHROMOSOME-6

Citation
C. Penhagoncalves et al., TYPE-1 DIABETES AND THE CONTROL OF DEXAMETHAZONE-INDUCED APOPTOSIS INMICE MAPS TO THE SAME REGION ON CHROMOSOME-6, Genomics, 28(3), 1995, pp. 398-404
Citations number
29
Categorie Soggetti
Genetics & Heredity
Journal title
ISSN journal
08887543
Volume
28
Issue
3
Year of publication
1995
Pages
398 - 404
Database
ISI
SICI code
0888-7543(1995)28:3<398:TDATCO>2.0.ZU;2-J
Abstract
Quantitative trait loci mapping was used to identify the chromosomal l ocation of genes that contribute to increase the resistance to apoptos is induced in immature CD4(+)8(+) thymocytes. An F2 intercross of the nonobese diabetic (NOD) mouse (displaying an apoptosis-resistance phen otype) and the C57BL/6 mouse (displaying a nonresistance phenotype) wa s phenotypically analyzed and genotyped for 32 murine microsatellite p olymorphisms. Maximum Likelihood methods identified a region on the di stal part of chromosome 6 that is linked to dexamethazone-induced apop tosis (led score = 3.46) and accounts for 14% of the phenotypic variat ion. This chromosomal region contains the diabetes susceptibility locu s Idd6, suggesting that the apoptosis-resistance phenotype constitutes a pathogenesis factor in IDDM of NOD mice. (C) 1995 Academic Press, I nc.