Klöting I, Schmidt S, Kovacs P
Department of Laboratory Animal Science, University of Greifswald, Karlsburg, Germany.
Biochem Biophys Res Commun. 1998 Apr 17;245(2):483-6. doi: 10.1006/bbrc.1998.8464.
By several crossing studies it has been demonstrated that the MHC class-II genes of the RT1u haplotype, Iddm1, and the lymphopenia, Iddm2, are essential, but not sufficient for diabetes development in the BB rat. Using diabetic BB/OK and diabetes-resistant DA rats it has been shown that a third non-MHC gene, Iddm3, on chromosome 18 cosegregates with diabetes in the BB/OK rat subline. Because mapping results need not be consistent among different crosses, we genetically analysed a new cross population using diabetic BB/OK and diabetes-resistant SHR/Mol rats analysing 73 microsatellite markers. The genetic analysis of Iddm1 and Iddm2 homozygous [(BB/OK x SHR)F1 x BB/OK] first backcross hybrids (BC1) confirmed the action of Iddm3 and one predisposing non-MHC locus, Iddm4, near Ighe/D6Mgh2 on chromosome 6 and one protective locus, Iddm5r(esistance), detected around Igf2/Tnt on chromosome 1. From these novel findings it is concluded that the diabetogenic phenotype of the BB/OK rat subline is the result of the interaction of predisposing and protecting diabetes genes.
通过多项杂交研究已证明,RT1u单倍型的MHC-II类基因Iddm1以及淋巴细胞减少症相关基因Iddm2对BB大鼠的糖尿病发展至关重要,但并不充分。利用糖尿病BB/OK大鼠和抗糖尿病的DA大鼠已表明,位于18号染色体上的第三个非MHC基因Iddm3在BB/OK大鼠亚系中与糖尿病共分离。由于不同杂交组合的定位结果不一定一致,我们使用糖尿病BB/OK大鼠和抗糖尿病的SHR/Mol大鼠对一个新的杂交群体进行了遗传分析,分析了73个微卫星标记。对Iddm1和Iddm2纯合子[(BB/OK×SHR)F1×BB/OK]第一代回交杂种(BC1)的遗传分析证实了Iddm3的作用以及一个位于6号染色体上靠近Ighe/D6Mgh2的易感非MHC基因座Iddm4和一个在1号染色体上围绕Igf2/Tnt检测到的保护基因座Iddm5r(抗性)。从这些新发现可以得出结论,BB/OK大鼠亚系的致糖尿病表型是易感和保护糖尿病基因相互作用的结果。