Gelinas C, Masse S, Bastin M
J Virol. 1984 Jul;51(1):242-6. doi: 10.1128/JVI.51.1.242-246.1984.
The DNA from polyomavirus mlt mutant P155 transforms cells in culture as efficiently as wild-type DNA but has a much lower tumorigenic potential when injected into newborn rodents. The mutant has a 12-base-pair deletion between nucleotides 1347 and 1360, i.e., in a region which encodes parts of the middle and large T antigens (G elinas et al., J. Virol. 43:1072-1081, 1982). To determine which of the two viral gene functions was affected by the mutation, we transferred the latter into a modified polyomavirus genome encoding exclusively the middle T protein. Our results show that the P155 mutation alters a function of the polyomavirus middle T protein required for the induction of the tumorigenic process in vivo. Beside the 12-base-pair deletion at 96.3 map units, there is no other alteration in the coding sequence of P155 middle T with respect to that of P16, the wild-type parental strain. We conclude, therefore, that the deletion is the lesion affecting the tumorigenic potential of mutant P155 .
多瘤病毒mlt突变体P155的DNA在培养中转化细胞的效率与野生型DNA一样高,但注射到新生啮齿动物体内时致瘤潜力要低得多。该突变体在核苷酸1347和1360之间有一个12个碱基对的缺失,即在一个编码中T抗原和大T抗原部分的区域(G·埃利纳斯等人,《病毒学杂志》43:1072 - 1081,1982年)。为了确定两种病毒基因功能中的哪一种受到了突变的影响,我们将后者转移到一个仅编码中T蛋白的修饰多瘤病毒基因组中。我们的结果表明,P155突变改变了多瘤病毒中T蛋白在体内诱导致瘤过程所需的一种功能。除了在96.3图谱单位处有12个碱基对的缺失外,P155中T的编码序列相对于野生型亲代菌株P16没有其他改变。因此,我们得出结论,该缺失是影响突变体P155致瘤潜力的损伤。