Nichol S T, Penn C R, Mahy B W
J Gen Virol. 1981 Dec;57(Pt 2):407-13. doi: 10.1099/0022-1317-57-2-407.
Eleven temperature-sensitive (ts) mutants of influenza A (fowl plague, Rostock) virus were analysed for in vitro RNA transcriptase activity in reactions primed by ApG or globin mRNA at 31 degrees C or at 40.5 degrees C, the restrictive temperature for ts mutant growth. Only those ts mutants studied which were defective in RNA segment 1, coding for the virion P2 protein, were defective in RNA transcriptase activity when compared to wild-type virus. Mutants having a defect in the P2 protein had no significant RNA transcriptase activity in reactions at 40.5 degrees C primed by globin mRNA. However, one mutant showed RNA transcriptase activity similar to wild-type virus at 40.5 degrees C when ApG (0.3 mM) was used as primer. The results suggest that influenza (fowl plague, Rostock) P2 protein is directly involved in the mRNA priming reaction, as well as in the RNA transcription reaction in vitro.
对甲型流感(禽瘟,罗斯托克株)病毒的11个温度敏感(ts)突变体进行了分析,以研究其在31℃或40.5℃(ts突变体生长的限制温度)下,由ApG或珠蛋白mRNA引发的反应中的体外RNA转录酶活性。与野生型病毒相比,只有那些在编码病毒粒子P2蛋白的RNA片段1中存在缺陷的ts突变体,其RNA转录酶活性才存在缺陷。在40.5℃由珠蛋白mRNA引发的反应中,P2蛋白存在缺陷的突变体没有显著的RNA转录酶活性。然而,当使用ApG(0.3 mM)作为引物时,有一个突变体在40.5℃下显示出与野生型病毒相似的RNA转录酶活性。结果表明,甲型流感(禽瘟,罗斯托克株)P2蛋白直接参与体外mRNA引发反应以及RNA转录反应。