Taylor B A, Meier H, Myers D D
Proc Natl Acad Sci U S A. 1971 Dec;68(12):3190-4. doi: 10.1073/pnas.68.12.3190.
Genetic studies were aimed at elucidation of the mechanism of inheritance of the group-specific antigen of the murine leukemia virus. Two approaches have been used. First, a classical Mendelian hybridization experiment was performed with mice of the high-leukemia AKR strain and the low-leukemia C57L strain; the first filial (F(1)) generation hybrids, the second filial (F(2)) generation hybrids, and the backcrosses to the two parental strains. Second, a number of partially inbred lines derived from the F(2) generation of the same cross were used. The results of these studies demonstrate a specific genetic regulation of expression of group-specific antigens. Genes permissive to the expression of the antigen are dominant or semidominant to their nonpermissive alleles. It appears that two dominant genes carried by the AKR strain, but not by the C57L strain, are necessary for the presence of a complete virus; one of these controls the expression of group-specific antigen.
遗传学研究旨在阐明鼠白血病病毒群特异性抗原的遗传机制。采用了两种方法。第一,用高白血病AKR品系和低白血病C57L品系的小鼠进行经典的孟德尔杂交实验;第一代(F(1))杂种、第二代(F(2))杂种,以及与两个亲本品系的回交。第二,使用了来自同一杂交组合F(2)代的一些部分近交系。这些研究结果证明了群特异性抗原表达的特定遗传调控。允许抗原表达的基因对其不允许表达的等位基因是显性或半显性的。似乎AKR品系携带但C57L品系不携带的两个显性基因是完整病毒存在所必需的;其中一个控制群特异性抗原的表达。