Whitaker P A, Yamada Y, Nakada D
J Virol. 1975 Dec;16(6):1380-90. doi: 10.1128/JVI.16.6.1380-1390.1975.
Bacteriophage T7 is unable to productively infect Escherichia coli strains carrying the sex factor F. T7 phage development, in terms of RNA and protein synthesis, was compared in T7-infected isogenic F- and F+ strains of E. coli. Slightly less T7 early mRNA and early protein were synthesized in F+ cells. In addition to the defect in T7 late protein production in F+ cells reported by others, significantly less T7 late mRNA was synthesized, about one-half of that produced in T7-infected F- cells. Moreover, host RNA synthesis was not completely inhibited. The protein-synthesizing ability of T7-infected F+ cells decayed much faster than that of F- cells both in vivo and in vitro. This faster decay appears to explain the failure of F+ cells to produce T7 late protein in vivo, even in the presence of a considerable amount of translatable T7 late mRNA. Therefore, it may not be necessary to postulate the involvement of specific translational discrimination against T7 late mRNA, although it appears that F-factor-mediated restriction of T7 involves changes in transcription as well as translation.
噬菌体T7无法有效感染携带性因子F的大肠杆菌菌株。在T7感染的大肠杆菌同基因F - 和F + 菌株中,就RNA和蛋白质合成而言,对T7噬菌体的发育情况进行了比较。F + 细胞中合成的T7早期mRNA和早期蛋白质略少。除了其他人报道的F + 细胞中T7晚期蛋白质产生缺陷外,合成的T7晚期mRNA也显著减少,约为T7感染的F - 细胞中产生量的一半。此外,宿主RNA合成并未被完全抑制。在体内和体外,T7感染的F + 细胞的蛋白质合成能力比F - 细胞衰退得快得多。这种更快的衰退似乎解释了即使存在大量可翻译的T7晚期mRNA,F + 细胞在体内仍无法产生T7晚期蛋白质的原因。因此,尽管F因子介导的对T7的限制似乎涉及转录和翻译的变化,但可能没有必要假设存在针对T7晚期mRNA的特定翻译歧视。