Polyoma-induced stimulation of nucleoplasmic transcription is paralleled by development of resistance against actinomycin D.

Polyoma virus induced in quiescent, Go-arrested mouse kidney cells a lytic infection. Synthesis of the polyoma T-antigens began 7-8 h after infection and was followed by a mitotic reaction of the host cell comprising stimulated synthesis and accumulation of cellular (mainly ribosomal) RNA and protein and duplication of the host cell chromatin (S-phase). In the present work we focused attention on nucleoplasmic transcription, i.e. synthesis of hnRNA, 5S RNA and tRNA. To inhibit selectively nucleolar transcription we used low concentrations of actinomycin D (act. D). Synthesis of 45S precursor- ribosomal RNA in mock- and polyoma-infected mouse kidney cells was completely blocked by 0.05 micrograms/ml act.D within 2 h. In mock-infected cells also nucleoplasmic transcription was rather sensitive against 0.05 micrograms/ml act.D. Polyoma- induced stimulation of nucleoplasmic transcription began around 12 h and was paralleled by the development of resistance against act.D. Resistance of nucleoplasmic transcription in virus-infected cells was thus similar to that observed by others in uninfected, proliferating mammalian cells. The possible biological implications of these results are discussed.