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 α-amanitin. In the latter, resistance is due to a mutation in RNA polymerase II. The toxin profoundly reduces synthesis of virus-specified polypeptides and morphopoiesis 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 γ 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.
|Number of pages
|Proceedings of the National Academy of Sciences of the United States of America
|Published - 1979
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