Li R, Botchan M R
Department of Molecular and Cell Biology, University of California, Berkeley 94720.
Proc Natl Acad Sci U S A. 1994 Jul 19;91(15):7051-5. doi: 10.1073/pnas.91.15.7051.
The papillomavirus E2 transcription factor is directly involved in viral DNA replication. Previous studies have shown that E2 interacts with both the viral E1 helicase and cellular replication proteins, and thus it may facilitate their targeting to the origin of replication. We demonstrate here that E1-mediated replication of bovine papillomavirus type 1 is repressed by nucleosomal assembly. The E2 protein counteracts this repression, and such activation requires the E2-binding sites adjacent to the origin of replication. These in vitro results are consistent with the previous in vivo findings that both E2 and specific E2 binding to DNA are absolutely required for replication of bovine papillomavirus. Furthermore, the function of E2 in preventing nucleosome-mediated repression can be achieved as well by several other acidic transcription factors. These data therefore strongly support the idea that a group of enhancer proteins may utilize similar mechanisms to stimulate transcription and replication.
乳头瘤病毒E2转录因子直接参与病毒DNA复制。先前的研究表明，E2与病毒E1解旋酶和细胞复制蛋白相互作用，因此它可能促进它们靶向复制起点。我们在此证明，1型牛乳头瘤病毒的E1介导的复制受到核小体组装的抑制。E2蛋白可抵消这种抑制作用，而这种激活需要靠近复制起点的E2结合位点。这些体外实验结果与先前的体内研究结果一致，即E2以及E2与DNA的特异性结合对于牛乳头瘤病毒的复制是绝对必需的。此外，其他几种酸性转录因子也能实现E2在防止核小体介导的抑制方面的功能。因此，这些数据有力地支持了这样一种观点，即一组增强子蛋白可能利用类似的机制来刺激转录和复制。
