Sköld O
J Virol. 1970 Jun;5(6):718-25. doi: 10.1128/JVI.5.6.718-725.1970.
Amino acid control of ribonucleic acid (RNA) synthesis in bacteria is known to be governed genetically by the rel locus. We investigated whether the rel gene of the host would also exert its effect on the regulation of phage-specific RNA synthesis in T4 phage-infected Escherichia coli cells. Since T-even phage infection completely shuts off host macromolecular synthesis, phage RNA synthesis could be followed specifically by the cumulative incorporation of radioactivity from labeled precursors into RNA of infected cells. Labeled uracil was shown to accumulate in phage-specific RNA for 30 to 35 min after infection, a phenomenon which probably reflects an expansion of the labile phage-RNA pool. Amino acid starvation was effected by the use of auxotrophic bacterial strains or thienylalanine. The latter substance is an amino acid analogue which induces a chemical auxotrophy by inhibiting the biosynthesis of phenylalanine, tyrosine, and tryptophan. Phage RNA synthesis was strictly dependent on the presence of amino acids, whereas phage deoxyribonucleic acid synthesis was not. By the use of several pairs of bacterial strains which were isogenic except for the rel gene, it was demonstrated that amino acid dependence was related to the allelic state of this gene. If the rel gene was mutated, amino acid starvation did not restrict phage RNA synthesis.
已知细菌中核糖核酸(RNA)合成的氨基酸控制受rel位点的遗传调控。我们研究了宿主的rel基因是否也会对T4噬菌体感染的大肠杆菌细胞中噬菌体特异性RNA合成的调控产生影响。由于T偶数噬菌体感染会完全关闭宿主大分子合成,因此可以通过将标记前体的放射性累积掺入感染细胞的RNA中,来特异性追踪噬菌体RNA合成。结果显示,标记的尿嘧啶在感染后30至35分钟内会在噬菌体特异性RNA中积累,这一现象可能反映了不稳定的噬菌体RNA池的扩大。通过使用营养缺陷型细菌菌株或噻吩丙氨酸来实现氨基酸饥饿。后者是一种氨基酸类似物,通过抑制苯丙氨酸、酪氨酸和色氨酸的生物合成来诱导化学营养缺陷。噬菌体RNA合成严格依赖于氨基酸的存在,而噬菌体脱氧核糖核酸合成则不然。通过使用除rel基因外其他基因相同的几对细菌菌株,证明了氨基酸依赖性与该基因的等位状态有关。如果rel基因发生突变,氨基酸饥饿不会限制噬菌体RNA合成。