Expression of a truncated viral trans-activator selectively impedes lytic infection by its cognate virus.
A virion protein of herpes simplex virus type 1 (HSV-1) specifically and potently activates transcription of the viral immediate early genes. Appropriate function of this protein, termed VP16, depends on an acidic transcriptional activation domain located within the 78 carboxyl-terminal amino acids of the protein. Mutated forms of the protein lacking this acidic domain lose the ability to activate transcription, and can dominantly interfere with the trans-activation function of native VP16 (ref. 1). We have prepared stably transformed mouse L cells that constitutively express a form of VP16 lacking its acidic activating domain. In this report we show that these cells are selectively impaired in their capacity to support the lytic infectious cycle of HSV-1, and that this impairment results from their inability to support immediate early transcription.
Friedman
A D
AD
Department of Embryology, Carnegie Institution of Washington, Baltimore, Maryland 21210.
Triezenberg
S J
SJ
McKnight
S L
SL
D000818:Animals; D005786:Gene Expression Regulation; D011558:Herpesvirus 1, Suid / Q000254:growth & development; D007700:Kinetics; D007739:L Cells; D051379:Mice; D009154:Mutation; D010750:Phosphoproteins / Q000096:biosynthesis / Q000502:physiology*; D010957:Plasmids; D018139:Simplexvirus / Q000235:genetics* / Q000472:pathogenicity; D015534:Trans-Activators; D014158:Transcription, Genetic; D014162:Transfection; D014762:Viral Interference; D014764:Viral Proteins / Q000096:biosynthesis / Q000502:physiology*
D010750:Phosphoproteins; D015534:Trans-Activators; D014764:Viral Proteins