Transactivation of a late herpes simplex virus promoter.
We have asked whether the promoter for the gene encoding the major capsid protein (VP5) of herpes simplex virus functions in uninfected mouse cells. Our experimental strategy was to first fuse the VP5 promoter to the herpes simplex virus thymidine kinase (TK) structural sequence and then to use the resulting hybrid gene to transform TK- cells to TK+. The recombinant gene transferred TK at an extremely low frequency by comparison with the wild-type TK gene, and the TK transcripts present within the resulting rare transformants initiated within the TK structural gene, rather than in the vicinity of the VP5 promoter. However, after infection with herpes simplex virus, large amounts of RNA driven from the VP5 promoter accumulated. We conclude that the VP5 promoter does not function in uninfected cells but is efficiently activated by virally coded factors, most likely one or more immediate-early proteins.
D000818:Animals; D001483:Base Sequence; D002213:Capsid / Q000235:genetics*; D004262:DNA Restriction Enzymes; D004789:Enzyme Activation; D005796:Genes; D005814:Genes, Viral; D007700:Kinetics; D007739:L Cells / Q000201:enzymology; D051379:Mice; D009154:Mutation; D009876:Operon; D010957:Plasmids; D018139:Simplexvirus / Q000235:genetics*; D013937:Thymidine Kinase / Q000172:deficiency / Q000235:genetics
D013937:Thymidine Kinase; D004262:DNA Restriction Enzymes