Repression of bovine papilloma virus replication is mediated by a virally encoded trans-acting factor.
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.
D052688:Bovine papillomavirus 1 / Q000235:genetics*; D004261:DNA Replication; D004279:DNA, Viral / Q000235:genetics; D005784:Gene Amplification; D005814:Genes, Viral; D027383:Papillomaviridae / Q000235:genetics*; D010957:Plasmids; D012093:Replicon; D012097:Repressor Proteins / Q000502:physiology*; D014157:Transcription Factors / Q000502:physiology*; D014764:Viral Proteins / Q000502:physiology*; D014779:Virus Replication
D004279:DNA, Viral; D012097:Repressor Proteins; D014157:Transcription Factors; D014764:Viral Proteins