Alwine J C, Picardi J
J Virol. 1986 Nov;60(2):400-4. doi: 10.1128/JVI.60.2.400-404.1986.
We used chloramphenicol acetyltransferase transient expression to examine the activity of the promoter elements of the simian virus 40 late promoter in the absence of large T antigen. Since the experiments were done in permissive CV-1 cells, these conditions mimic the state which exists early in the viral lytic cycle before the onset of replication and T-antigen-mediated trans activation. Our data, using deletion analysis, indicate that removal of the 21-base-pair (bp) repeat region causes as much as a 10-fold increase in activity of the late promoter elements. This result suggests that the 21-bp repeat sequences may be involved in repression of the late promoter elements during the early phase of the lytic infection. This is supported by competition analysis which indicates that increasing amounts of competitor containing only the 21-bp repeat region results in increased activity of the intact promoter. A model for the activity of the late promoter through the course of lytic infection is presented.
我们使用氯霉素乙酰转移酶瞬时表达来检测在没有大T抗原的情况下猿猴病毒40晚期启动子的启动子元件的活性。由于实验是在允许性CV-1细胞中进行的，这些条件模拟了病毒裂解周期早期在复制开始和T抗原介导的反式激活之前存在的状态。我们使用缺失分析的数据表明，去除21个碱基对（bp）的重复区域会导致晚期启动子元件的活性增加多达10倍。这一结果表明，21 bp的重复序列可能在裂解感染的早期阶段参与了对晚期启动子元件的抑制。竞争分析支持了这一点，该分析表明，仅含有21 bp重复区域的竞争者数量增加会导致完整启动子的活性增加。本文提出了一个关于裂解感染过程中晚期启动子活性的模型。
