Huh N E, Weaver R F
Department of Biochemistry, University of Kansas, Lawrence 66045.
J Gen Virol. 1990 Jan;71 ( Pt 1):195-201. doi: 10.1099/0022-1317-71-1-195.
Nuclear run-on assays carried out in the presence and absence of the RNA polymerase II inhibitor, alpha-amanitin, were used to determine the exact timing of the switch from inhibitor-sensitive transcription catalysed by host RNA polymerase II, to inhibitor-resistant transcription catalysed by the baculovirus-induced RNA polymerase. These studies revealed that the onset of alpha-amanitin-resistant transcription is just after 6 h post-infection, simultaneous with the beginning of the late phase of infection. They also showed that transcripts from the p26 gene in the HindIII Q/P region and the p35 gene in the HindIII K/Q region of the viral genome are synthesized by the host RNA polymerase II both early and late in infection. On the other hand, transcripts of the p10 gene in the HindIII Q/P region and the gamma transcripts in the HindIII K region are synthesized by the alpha-amanitin-resistant, virus-induced RNA polymerase late in infection.
在存在和不存在RNA聚合酶II抑制剂α-鹅膏蕈碱的情况下进行的核运行分析,用于确定从宿主RNA聚合酶II催化的抑制剂敏感转录,转变为杆状病毒诱导的RNA聚合酶催化的抑制剂抗性转录的确切时间点。这些研究表明,α-鹅膏蕈碱抗性转录的起始时间是在感染后6小时刚过,与感染后期的开始同时发生。它们还表明,病毒基因组HindIII Q/P区域中的p26基因和HindIII K/Q区域中的p35基因的转录本在感染的早期和晚期均由宿主RNA聚合酶II合成。另一方面,HindIII Q/P区域中的p10基因的转录本和HindIII K区域中的γ转录本在感染后期由α-鹅膏蕈碱抗性的、病毒诱导的RNA聚合酶合成。