Tseng R W, Fujimura F K
Cancer Research Center, La Jolla Cancer Research Foundation, California 92037.
J Virol. 1988 Aug;62(8):2890-5. doi: 10.1128/JVI.62.8.2890-2895.1988.
A point mutation at nucleotide 5258 in the B enhancer of the polyomavirus host range mutant F441 leads to productive infection of F9 embryonal carcinoma cells, which are refractory to infection by wild-type polyomavirus. Specific oligonucleotides were used to construct mutations in two other potentially important domains within the B enhancer of F441 DNA. One of these domains is the binding site for a factor present in nuclear extracts of F9 cells, and the other is a region that has sequence similarity to putative core sequences observed in a number of different viral enhancers. Mutation within either of these two domains, even in the presence of the F441 mutation, was detrimental to polyomavirus enhancer activity in F9 cells, as determined by both transfection and infection assays.
多瘤病毒宿主范围突变体F441的B增强子中核苷酸5258处的点突变导致F9胚胎癌细胞产生有 productive 感染，而野生型多瘤病毒无法感染F9胚胎癌细胞。使用特定的寡核苷酸在F441 DNA的B增强子内的另外两个潜在重要结构域中构建突变。其中一个结构域是F9细胞核提取物中存在的一种因子的结合位点，另一个结构域是与许多不同病毒增强子中观察到的推定核心序列具有序列相似性的区域。通过转染和感染试验确定，即使在存在F441突变的情况下，这两个结构域中任何一个发生突变都会损害F9细胞中的多瘤病毒增强子活性。
