Berg L, Lusky M, Stenlund A, Botchan M R
Cell. 1986 Aug 29;46(5):753-62. doi: 10.1016/0092-8674(86)90351-x.
Cells transformed with bovine papilloma virus type 1 mutants in the E6 or E6/7 genes are resistant to high-copy-number amplification of wild-type DNA after supertransfection. Transient and stable replication assays demonstrate this effect. If the supertransfected DNA has a mutation in a newly defined gene (M), this cellular immunity to high-copy-number replication is overcome, resulting in transient replication of the input DNA. In contrast, the resident plasmid does not participate in amplification and is maintained at a constant low copy number. Cotransformation of M- mutants and wild-type DNA into these cells leads to shutoff of replication of both genomes. Thus, M- mutants define a trans-acting negative modulator that regulates viral replication. This function is distinct from the positive factors required for replication. We propose a model that explains why the loss of E6 and E6/7 function leads to immunity of the infected cell.
用1型牛乳头瘤病毒E6或E6/7基因的突变体转化的细胞在超转染后对野生型DNA的高拷贝数扩增具有抗性。瞬时和稳定复制试验证明了这种效应。如果超转染的DNA在一个新定义的基因（M）中发生突变，这种对高拷贝数复制的细胞免疫就会被克服，导致输入DNA的瞬时复制。相比之下，常驻质粒不参与扩增，而是维持在恒定的低拷贝数。将M-突变体和野生型DNA共转化到这些细胞中会导致两个基因组的复制关闭。因此，M-突变体定义了一种调节病毒复制的反式作用负调节因子。该功能不同于复制所需的正因子。我们提出了一个模型来解释为什么E6和E6/7功能的丧失会导致受感染细胞产生免疫。
