Abstract
The participation of host RNA polymerase II in the vaccinia life cycle was examined by comparing efficiency of multiplication after treating the Ama+ sensitive and Ama 102 drug resistant lines with alpha-amanitin. In the latter, resistance is due to a mutation in RNA polymerase II. The toxin profoundly reduces synthesis of virus-specified polypeptides and morphopoeisis in Ama+ but not in Ama 102 rat myoblasts without appreciably altering vaccinia DNA replication in either cell type. This implicates RNA polymerase II in the expression of late virus functions. Circumstantial evidence from a model system indicates that gamma irradiation of the host prior to infection might disrupt transcription into functional mRNA from the nucleus. Irradiation does not, however, alter the capability of the host to support vaccinia multiplication fully. Therefore, ongoing host nuclear transcription may not be required by this virus. The above results are consistent with the ability of cytoplasts to produce small quantities of mature progeny. Our studies lead us to hypothesize that RNA polymerase II or a subunit of the host enzyme may participate directly in late transcription of the vaccinia genome.
MeSH Terms
Amanitins/pharmacology
Animals
DNA-Directed RNA Polymerases/metabolism
Dactinomycin/pharmacology
Gamma Rays
Hemagglutinins, Viral/genetics
L Cells
Mice
RNA Polymerase II/metabolism
Transcription, Genetic/drug effects
Vaccinia virus/genetics
Vesicular stomatitis Indiana virus/genetics
Viral Proteins/biosynthesis
Virus Replication/drug effects,radiation effects
Chemicals
Amanitins
Hemagglutinins, Viral
Viral Proteins
Dactinomycin
RNA Polymerase II
DNA-Directed RNA Polymerases
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Silver M
McFadden G
Wilton S
Dales S
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