Matter J M, Khandjian E W, Weil R
Nucleic Acids Res. 1983 Feb 25;11(4):1039-58. doi: 10.1093/nar/11.4.1039.
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.
多瘤病毒在静止的、处于G0期的小鼠肾细胞中引发了溶细胞感染。感染后7-8小时开始合成多瘤T抗原，随后宿主细胞发生有丝分裂反应，包括细胞（主要是核糖体）RNA和蛋白质的合成与积累增加以及宿主细胞染色质的复制（S期）。在本研究中，我们将注意力集中在核质转录上，即不均一核RNA（hnRNA）、5S RNA和转运RNA（tRNA）的合成。为了选择性抑制核仁转录，我们使用了低浓度的放线菌素D（act.D）。在模拟感染和多瘤病毒感染的小鼠肾细胞中，0.05微克/毫升的act.D在2小时内完全阻断了45S前体核糖体RNA的合成。在模拟感染的细胞中，核质转录对0.05微克/毫升的act.D也相当敏感。多瘤病毒诱导的核质转录刺激在大约12小时开始，并伴随着对act.D抗性的发展。因此，病毒感染细胞中核质转录的抗性与其他研究中在未感染的增殖哺乳动物细胞中观察到的抗性相似。讨论了这些结果可能的生物学意义。
