Abstract
Several biologically distinguishable type-C RNA viruses are genetically transmitted in mouse cells. In the present report, chemicals that inhibit several different steps in protein synthesis are shown to cause marked increases in the cellular concentration of virus-specific RNA and the subsequent induction of virus. Analysis of the effect of translational inhibitors on mouse embryo cells of different genotypes indicates that activation of viral RNA is specific for one endogenous virus class and is a dominant genetic characteristic. Two lines of evidence favor the hypothesis that the induction of viral RNA involves transcriptional derepression rather than an alteration in its post-transcriptional processing. First, nuclear and cytoplasmic fractions of induced cells are shown to demonstrate similar increases in their concentrations of virus-specific RNA. Second, the decay of induced viral RNA following inhibition of further RNA synthesis by actinomycin D is not prevented by continued exposure to the inducer. These findings weigh heavily against the possibility that translational inhibitors act to stabilize viral RNA post-transcriptionally. The results are consistent with a model in which the expression of one class of endogenous virus is regulated by a labile repressor protein acting at a transcriptional level.