Salomon C, Türler H, Weil R
Nucleic Acids Res. 1977;4(5):1483-503. doi: 10.1093/nar/4.5.1483.
We studied synthesis of viral and cellular RNA in the presence and absence of 5-fluorodeoxyuridine (FdU, an inhibitor of DNA synthesis) during lytic infection with polyoma virus in confluent, primary mouse kidney cell cultures. In the presence of FdU, synthesis of early 19S polyoma mRNA and of polyoma tumor (T)-antigen, i.e. expression of the early viral gene, is rapidly followed by a mitogenic reaction of the host cell; it leads to an increase of 30 +/- 5% in cellular, mainly 28S and 18S rRNA, followed by activation of the cellular DNA-synthesizing apparatus. Polyoma-induced cellular RNA synthesis is paralleled by increased production of early 19S mRNA and begin of expression of the late viral genes, leading to synthesis of small amounts of late 19S and 16S mRNAs. Changed expression of the viral genome occurs in the absence of detectable synthesis of polyoma DNA I. Infection in the absence of FdU induces the same sequence of events; it is followed, however, by duplication of the mouse cell chromatin (S-phase) and production of progeny virus.
我们研究了在融合的原代小鼠肾细胞培养物中,多瘤病毒裂解感染期间,在有和没有5-氟脱氧尿苷(FdU,一种DNA合成抑制剂)存在的情况下病毒和细胞RNA的合成。在FdU存在的情况下,早期19S多瘤病毒mRNA和多瘤病毒肿瘤(T)抗原的合成,即早期病毒基因的表达,会迅速引发宿主细胞的有丝分裂反应;这导致细胞内主要是28S和18S rRNA增加30±5%,随后激活细胞DNA合成装置。多瘤病毒诱导的细胞RNA合成与早期19S mRNA产量增加以及晚期病毒基因开始表达同时发生,导致合成少量晚期19S和16S mRNA。在没有可检测到的多瘤病毒DNA I合成的情况下,病毒基因组的表达发生了变化。在没有FdU的情况下感染会引发相同的事件序列;然而,随后会出现小鼠细胞染色质的复制(S期)和子代病毒的产生。