Hayashi M N, Hayashi M, Imai M
J Virol. 1981 Apr;38(1):198-207. doi: 10.1128/JVI.38.1.198-207.1981.
A previous report (Hayashi et al., Proc. Natl. Acad. Sci. U.S.A. 73:3519-3523, 1976) indicated that in vivo bacteriophage phi X174 mRNA's terminate after genes J, F, G, and H. However, termination at these sites is not stringent. To determine whether termination of phi X174 transcription depends on rho factor activity, we introduced a temperature-sensitive rho mutation (nitA) into a phi X174-sensitive host cell line and determined termination sites in wild-type and nitA cells. We found that (i) normal phi X174 terminators were recognized in phi X174-infected nitA cells, (ii) the rho mutation relieved polar effects caused by nonsense mutations in the phage genome or by chloramphenicol treatment of the host cells, and (iii) polarity was not caused by premature termination of transcription at the site of the polar mutation. RNA synthesis continued beyond the site to the first rho-sensitive site.
先前的一份报告(林等,《美国国家科学院院刊》73:3519 - 3523,1976年)表明,体内噬菌体φX174的信使核糖核酸在基因J、F、G和H之后终止。然而,在这些位点的终止并不严格。为了确定φX174转录的终止是否依赖于ρ因子活性,我们将一个温度敏感型ρ突变(nitA)导入一个对φX174敏感的宿主细胞系,并确定了野生型细胞和nitA细胞中的终止位点。我们发现:(i)在感染了φX174的nitA细胞中能识别正常的φX174终止子;(ii)ρ突变消除了由噬菌体基因组中的无义突变或宿主细胞经氯霉素处理所引起的极性效应;(iii)极性并非由极性突变位点处转录的过早终止所导致。RNA合成在该位点之后继续进行,直至第一个对ρ敏感的位点。