Liu Z, Carmichael G G
Department of Microbiology, University of Connecticut Health Center, Farmington 06030.
Proc Natl Acad Sci U S A. 1993 Sep 15;90(18):8494-8. doi: 10.1073/pnas.90.18.8494.
Early in infection of permissive mouse cells, messages from the early region of the polyoma virus genome accumulate preferentially over those from the late region. After initiation of DNA replication, the balance between early and late gene expression is reversed in favor of the late products. In previous work from our laboratory, we showed that viral early proteins do not activate the polyoma late promoter in the absence of DNA replication. Here we show that activation of the late genes in replication-incompetent viral genomes can occur if actively replicating genomes are present in the same cell. A low level of DNA replication, however, is insufficient to induce the early-late switch. Furthermore, replication-competent genomes that fail to accumulate late RNA molecules are defective in the transactivation of replication-incompetent genomes. We suggest that titration of an unknown diffusible factor(s) after DNA replication relieves the block to late RNA accumulation seen in the early phase, with most of this titration being attributable to late-strand RNA molecules themselves.
在允许性小鼠细胞感染早期，多瘤病毒基因组早期区域的信使优先于晚期区域的信使积累。DNA复制开始后，早期和晚期基因表达之间的平衡发生逆转，有利于晚期产物。在我们实验室之前的工作中，我们表明在没有DNA复制的情况下，病毒早期蛋白不会激活多瘤晚期启动子。在这里我们表明，如果同一细胞中存在活跃复制的基因组，复制无能力的病毒基因组中的晚期基因也可以被激活。然而，低水平的DNA复制不足以诱导早期-晚期转换。此外，未能积累晚期RNA分子的复制有能力的基因组在复制无能力的基因组的反式激活中存在缺陷。我们认为，DNA复制后对一种未知的可扩散因子的滴定缓解了早期阶段所见的对晚期RNA积累的阻碍，这种滴定的大部分归因于晚期链RNA分子本身。
