Butler A, Whitehead A S
Department of Genetics, Trinity College, University of Dublin, Ireland.
Scand J Immunol. 1994 Sep;40(3):355-8. doi: 10.1111/j.1365-3083.1994.tb03473.x.
We have tested the hypothesis that structural allelic variants of serum amyloid A confer relative resistance to secondary amyloidosis in the A/J mouse. F2 mice, previously generated from amyloid-resistant (A/J) and amyloid-susceptible (C57BL/6J) strains and categorized with respect to amyloid susceptibility, were genotyped by polymerase chain reaction (PCR) amplification of the polymorphic D7Nds5 microsatellite. This microsatellite is closely linked to the SAA gene cluster and can discriminate between D7Nds5 alleles of A/J and C57BL/6J origin. The distribution of D7Nds5 genotypes in relation to splenic amyloid load did not deviate significantly from that expected of a random distribution, indicating that A/J amyloid resistance is not determined by variants at, or close to, D7Nds5. Therefore, structural alleles in the tightly-linked SAA gene cluster do not confer amyloid resistance in this mouse model.
血清淀粉样蛋白A的结构等位基因变异赋予A/J小鼠对继发性淀粉样变性的相对抗性。先前由抗淀粉样变性（A/J）和易患淀粉样变性（C57BL/6J）品系培育出的F2小鼠，已根据淀粉样变性易感性进行了分类，并通过聚合酶链反应（PCR）扩增多态性D7Nds5微卫星进行基因分型。该微卫星与血清淀粉样蛋白A（SAA）基因簇紧密相连，能够区分A/J和C57BL/6J来源的D7Nds5等位基因。与脾脏淀粉样蛋白负荷相关的D7Nds5基因型分布与随机分布预期的情况没有显著差异，这表明A/J小鼠的抗淀粉样变性能力并非由D7Nds5处或其附近的变异所决定。因此，在这个小鼠模型中，紧密连锁的SAA基因簇中的结构等位基因并不能赋予抗淀粉样变性能力。
