Abstract
The herpes simplex virus thymidine kinase (TK) gene is transcriptionally activated in trans ("transactivated") by virus-encoded proteins during the infectious cycle. We show that TK plasmids introduced into a HeLa cell transient transcription assay system are also transactivated after infection with a TK- virus. Several aspects of this response are similar to regulation during the normal infectious cycle. Assay of TK promoter deletion and 5- to 10-base-pair substitution mutants in this system reveals that the transactivation response depends on the intactness of 109 base pairs of 5' gene flanking sequence. Differences between these results and analogous assays in the Xenopus oocyte system are discussed. A model for the putative binding of transactivator(s) to the promoter region is presented.
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