Stoltzfus C M, Dimock K, Horikami S, Ficht T A
J Gen Virol. 1983 Oct;64 (Pt 10):2191-202. doi: 10.1099/0022-1317-64-10-2191.
The stabilities of B77 avian sarcoma virus intracellular RNAs were compared to the stability of the total cellular poly(A)-containing RNA by labelling infected chicken embryo fibroblasts with [3H]uridine for 15 h, adding actinomycin D (1 microgram per ml) to block further transcription of viral RNA, and selecting virus-specific RNA from the total cellular poly(A)-containing RNA at 3 hourly intervals. The three virus-specific RNA species (9.3, 3.3 and 5.4 kilobases) decayed with half-lives of 7.5, 10, and 15 h, respectively, whereas the bulk of the cellular mRNA decayed with a half-life of 13 h. To correlate these decay rates with the disappearance of mRNA activities, the actinomycin D-treated cells were pulse-labelled with [3H]leucine at 3 hourly intervals after the addition of the drug and virus-specific protein synthesis was assayed by immunoprecipitation. The mRNA activity for the precursor to the non-glycosylated viral structural proteins (Pr76gag) decayed with a half-life of approximately 6 h, whereas the mRNA activity coding for the precursor to the envelope proteins (gPr92env) decayed with a half-life of 14 h. Thus, the rate of decay of the individual mRNA species corresponded reasonably well with the decay rate for the synthesis of two of the corresponding gene products. The results indicated that the 5.4 kb env mRNA is more stable under these conditions than the 9.3 kb gag mRNA but was not significantly more stable than the bulk of the cellular mRNA. Virus particle production following the addition of actinomycin D was determined by the reverse transcriptase assay and by the incorporation of viral genomic 70S RNA into extracellular virions. Both assays yielded similar results and indicated that particle production was inhibited at a rate (t 1/2 = 4 h) somewhat faster than the decay of Pr76gag synthesis or the disappearance of 9.3 kb RNA. It was established by two independent methods (pulse and chase, and approach to isotope equilibrium), however, that the intracellular half-life of the RNA that is packaged into virions is 6 to 7 h. Thus, these results suggest that a single metabolic pool of 9.3 kb RNA exists in avian sarcoma virus-infected cells and is used both as mRNA and as genome RNA.
通过用[³H]尿苷标记感染的鸡胚成纤维细胞15小时,添加放线菌素D(每毫升1微克)以阻断病毒RNA的进一步转录,并每隔3小时从总细胞含多聚腺苷酸的RNA中筛选病毒特异性RNA,比较了B77禽肉瘤病毒细胞内RNA的稳定性与总细胞含多聚腺苷酸RNA的稳定性。三种病毒特异性RNA种类(9.3、3.3和5.4千碱基)的半衰期分别为7.5、10和15小时,而大部分细胞mRNA的半衰期为13小时。为了将这些衰变率与mRNA活性的消失相关联,在添加药物后每隔3小时用[³H]亮氨酸对经放线菌素D处理的细胞进行脉冲标记,并通过免疫沉淀法测定病毒特异性蛋白质合成。非糖基化病毒结构蛋白(Pr76gag)前体的mRNA活性以约6小时的半衰期衰变,而编码包膜蛋白(gPr92env)前体的mRNA活性以14小时的半衰期衰变。因此,各个mRNA种类的衰变率与两种相应基因产物合成的衰变率相当吻合。结果表明,在这些条件下,5.4 kb的env mRNA比9.3 kb的gag mRNA更稳定,但并不比大部分细胞mRNA显著更稳定。添加放线菌素D后的病毒颗粒产生通过逆转录酶测定法以及病毒基因组70S RNA掺入细胞外病毒颗粒来确定。两种测定方法得出了相似的结果,并表明颗粒产生的抑制速率(t 1/2 = 4小时)比Pr76gag合成的衰变或9.3 kb RNA的消失稍快。然而,通过两种独立方法(脉冲追踪法和接近同位素平衡法)确定,包装到病毒颗粒中的RNA的细胞内半衰期为6至7小时。因此,这些结果表明,禽肉瘤病毒感染的细胞中存在一个单一的9.3 kb RNA代谢池,并用作mRNA和基因组RNA。