Evidence that herpes simplex virus DNA is transcribed by cellular RNA polymerase B.
In herpes simplex virus type 1 (HSV-1)-infected HEp-2 cells, amanitin added before or at various times after infection always reduced viral multiplication. Also, the three waves of transcription of HSV-1 DNA, which led to the synthesis of alpha, beta-, and gamma-polypeptides, were all sensitive to amanitin in HEp-2 cells, and the amanitin-sensitive RNA polymerase activities of isolated nuclei were equally sensitive to the inhibitor before and during the infection. On the contrary, HSV-1 DNA transcription was totally unaffected by amanitin in AR1/9-5B cells, a mutant subline of CHO cells that possesses an amanitin-resistant RNA polymerase B. Together, these results strongly suggest that HSV-1 DNA utilizes for its transcription a polymerase undistinguishable from host cell RNA polymerase B with respect to its sensitivity to amanitin.
D000546:Amanitins / Q000494:pharmacology; D002460:Cell Line; D002467:Cell Nucleus / Q000201:enzymology; D003513:Cycloheximide / Q000494:pharmacology; D004279:DNA, Viral / Q000378:metabolism*; D012321:DNA-Directed RNA Polymerases / Q000378:metabolism*; D009154:Mutation; D010452:Peptide Biosynthesis; D018139:Simplexvirus / Q000378:metabolism*; D014158:Transcription, Genetic; D014764:Viral Proteins / Q000096:biosynthesis
D000546:Amanitins; D004279:DNA, Viral; D014764:Viral Proteins; D003513:Cycloheximide; D012321:DNA-Directed RNA Polymerases