A single regulatory region modulates both cis activation and trans activation of the herpes simplex virus VP5 promoter in transient-expression assays in vivo.
A detailed analysis of the expression of the bacterial chloramphenicol acetyltransferase gene controlled by the herpes simplex virus major capsid protein (VP5) promoter showed that this promoter can be functionally separated into an 80-base core region, which has the minimal information required to serve as a pol II promoter but which is not fully activated by viral superinfection or by cotransfections with plasmids bearing functional alpha (immediate-early) genes, and an approximately 100-base regulatory region upstream of the core, which allowed full induction of VP5 promoter-driven chloramphenicol acetyltransferase activity but which repressed the ability of the VP5 core promoter to be cis activated by the simian virus 40 enhancer. This was in distinct contrast to the situation with the alkaline exonuclease promoter (a model early promoter) and defined the regions of this promoter which can be used to study the interaction between viral promoters and putative regulatory proteins induced by viral infection.
D000123:Acetyltransferases / Q000235:genetics; D002213:Capsid / Q000235:genetics*; D015500:Chloramphenicol O-Acetyltransferase; D004742:Enhancer Elements, Genetic; D005786:Gene Expression Regulation; D011401:Promoter Regions, Genetic; D018139:Simplexvirus / Q000235:genetics*; D014158:Transcription, Genetic; D014162:Transfection; D014764:Viral Proteins / Q000494:pharmacology
D014764:Viral Proteins; D000123:Acetyltransferases; D015500:Chloramphenicol O-Acetyltransferase