POLYGENIC CONTROL OF AUTOIMMUNE DIABETES IN NONOBESE DIABETIC MICE
POLYGENIC CONTROL OF AUTOIMMUNE DIABETES IN NONOBESE DIABETIC MICE
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DOI：
10.1038/ng0893-404
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发表时间：
1993-08-01
期刊：
影响因子：
30.8
通讯作者：
TODD, JA
中科院分区：
文献类型：
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作者：
GHOSH, S;PALMER, SM;TODD, JA
非肥胖（NOD）糖尿病小鼠基因组的部分排除作图显示糖尿病与至少五种不同的染色体连锁。我们现在已经排除了几乎所有基因组中存在的具有完全隐性效应的易感基因，并获得了10个不同位点与糖尿病或糖尿病前期病变胰岛炎连锁的证据，表明遗传的多基因模式。这些位点的相对重要性和它们之间的相互作用已被评估使用一个新的应用程序的多个polychotomous回归方法。与胰岛炎和糖尿病密切相关的候选疾病基因白细胞介素-2（IL-2）显示在NOD中具有不同的序列，包括在成熟蛋白中编码氨基酸重复的串联重复序列的插入和缺失。
Partial exclusion mapping of the nonobese (NOD) diabetic mouse genome has shown linkage of diabetes to at least five different chromosomes. We have now excluded almost all of the genome for the presence of susceptibility genes with fully recessive effects and have obtained evidence of linkage of ten distinct loci to diabetes or the prediabetic lesion, insulitis, indicative of a polygenic mode of inheritance. The relative importance of these loci and their interactions have been assessed using a new application of multiple polychotomous regression methods. A candidate disease gene, interleukin-2 (Il-2), which is closely linked to insulitis and diabetes, is shown to have a different sequence in NOD, including an insertion and a deletion of tandem repeat sequences which encode amino acid repeats in the mature protein.