Donini P
J Bacteriol. 1970 Jun;102(3):616-27. doi: 10.1128/jb.102.3.616-627.1970.
Starvation for a required amino acid of normal or RC(str)Escherichia coli infected with T-even phages arrests further synthesis of phage deoxyribonucleic acid (DNA). This amino acid control over phage DNA synthesis does not occur in RC(rel)E. coli mutants. Heat inactivation of a temperature-sensitive aminoacyl-transfer ribonucleic acid (RNA) synthetase similarly causes an arrest of phage DNA synthesis in infected cells of RC(str) phenotype but not in cells of RC(rel) phenotype. Inhibition of phage DNA synthesis in amino acid-starved RC(str) host cells can be reversed by addition of chloramphenicol to the culture. Thus, the general features of amino acid control over T-even phage DNA synthesis are entirely analogous to those known for amino acid control over net RNA synthesis of uninfected bacteria. This analogy shows that the bacterial rel locus controls a wider range of macromolecular syntheses than had been previously thought.
用T偶数噬菌体感染正常的或RC(str)大肠杆菌时,若缺乏一种必需氨基酸,会阻止噬菌体脱氧核糖核酸(DNA)的进一步合成。这种对噬菌体DNA合成的氨基酸控制在RC(rel)大肠杆菌突变体中不会发生。温度敏感型氨酰转移核糖核酸(RNA)合成酶的热失活同样会导致RC(str)表型感染细胞中噬菌体DNA合成的停滞,但不会导致RC(rel)表型细胞中噬菌体DNA合成的停滞。在缺乏氨基酸的RC(str)宿主细胞中,通过向培养物中添加氯霉素可以逆转噬菌体DNA合成的抑制。因此,氨基酸对T偶数噬菌体DNA合成的控制的一般特征与已知的氨基酸对未感染细菌净RNA合成的控制完全类似。这种相似性表明,细菌rel位点控制的大分子合成范围比以前认为的更广。