Logo image
Non-major histocompatibility complex-linked diabetes susceptibility loci on chromosomes 4 and 13 in a backcross of the DP-BB/Wor rat to the WF rat
Journal article   Peer reviewed

Non-major histocompatibility complex-linked diabetes susceptibility loci on chromosomes 4 and 13 in a backcross of the DP-BB/Wor rat to the WF rat

A M Martin, E P Blankenhorn, M N Maxson, M Zhao, J Leif, J P Mordes and D L Greiner
Diabetes (New York, N.Y.), v 48(1), pp 50-58
Jan 1999
PMID: 9892222

Abstract

Chromosomes, Human, Pair 13 - genetics Genetic Predisposition to Disease - genetics Rats, Inbred BB - genetics Major Histocompatibility Complex - genetics Humans Diabetes Mellitus, Type 1 - genetics Rats Genetic Linkage - drug effects Chromosome Mapping Pancreatitis - complications Chromosomes, Human, Pair 4 - genetics Disease Progression Pancreatitis - genetics Phenotype Rats, Inbred WF - genetics Animals Diabetes Mellitus, Type 1 - etiology Hybridization, Genetic Islets of Langerhans Genome Pancreatitis - physiopathology
BB rats are used as models of autoimmune human IDDM. Genetic control of IDDM in both species is complex, including both major histocompatibility complex (MHC)-linked and non-MHC-linked genes. DP-BB rats develop IDDM spontaneously. Expression of disease in these animals requires homozygosity at the lyp locus, which causes lymphopenia. All genetic analyses of BB rat diabetes to date have backcrossed to the DP-BB strain or used (DP-BB x non-BB)F2 animals to ensure that a fraction of progeny are homozygous for lyp. Here we report the analysis of a backcross of the DP-BB rat to the histocompatible WF rat. Neither WF nor (WF x DP-BB)F1 animals develop spontaneous IDDM. However, 95% of (WF x DP-BB)F1 rats and a fraction of (WF x DP-BB) x WF backcross animals readily develop IDDM after treatment with polyinosinic:polycytidylic acid and a cytotoxic anti-RT6.1 monoclonal antibody. Using simple sequence length polymorphism analysis, we have mapped loci on chromosomes 4 and 13 that show significant linkage to IDDM expression and insulitis. The susceptibility locus on chromosome 4 is linked to, but not identical to, lyp. We propose a disease model for the BB rat that requires 1) the RT1u MHC haplotype for disease susceptibility, 2) a new locus on chromosome 4 for disease initiation (as measured by insulitis), 3) a new locus on chromosome 13 for disease progression in response to environmental perturbation, and 4) lyp for spontaneous expression of disease.

Metrics

10 Record Views
45 citations in Scopus

Details

UN Sustainable Development Goals (SDGs)

This publication has contributed to the advancement of the following goals:

#3 Good Health and Well-Being

InCites Highlights

Data related to this publication, from InCites Benchmarking & Analytics tool:

Collaboration types
Domestic collaboration
Web of Science research areas
Endocrinology & Metabolism
Logo image