Freda C E, Cohen S S
J Bacteriol. 1966 Dec;92(6):1670-9. doi: 10.1128/jb.92.6.1670-1679.1966.
Freda, Celia E. (University of Pennsylvania School of Medicine, Philadelphia), and Seymour S. Cohen. Streptomycin and infection of Escherichia coli by T6r(+) bacteriophage. J. Bacteriol. 92:1670-1679. 1966.-The thymineless, histidineless, uracil-less Escherichia coli 15 THU was shown to be sensitive to streptomycin, dying in patterns comparable to that of strain 15 TAU in the presence or absence of the required amino acid histidine. In the absence of histidine, the antibiotic stimulated ribonucleic acid (RNA) synthesis without a detectable inhibition or stimulation of deoxyribonucleic acid (DNA) synthesis. In the presence of streptomycin (40mug/ml) under conditions of multiple infection with T6r(+), lysis of THU occurred 1 hr earlier than did the control, having produced about one-third as much DNA and phage as did the control. In the absence of histidine, thereby preventing synthesis of phage DNA, accumulation of virus-induced RNA was similar for about 30 min in control and streptomycin-treated systems. In the presence of the antibiotic, however, the infected cells accumulated about 50 to 70% more RNA than did the control after 90 min. Nevertheless, the turnover of RNA was not detectably affected by streptomycin. The rate of production and final amount of deoxycytidylate hydroxymethylase, as well as the cut off time of synthesis of this enzyme, were scarcely affected by streptomycin. The beginning of DNA synthesis was delayed about 3 to 4 min by the antibiotic. The incorporation of histidine in infected cells was unaffected for 10 min and was only about 10% less than the control at 70 min. Lysozyme production began at about 10 min in control and antibiotic-treated systems, continued at essentially similarly increasing rates for 20 min, but stopped abruptly in the streptomycin-treated cells despite continuing protein synthesis. With the exception of lysozyme, the production of phage-specific polymers in a streptomycin-sensitive bacterium was only slightly affected by the antibiotic.
弗雷达,西莉亚·E.(宾夕法尼亚大学医学院,费城),以及西摩·S. 科恩。链霉素与T6r(+)噬菌体对大肠杆菌的感染。《细菌学杂志》92:1670 - 1679。1966年。——无胸腺嘧啶、无组氨酸、无尿嘧啶的大肠杆菌15 THU被证明对链霉素敏感,在有或没有所需氨基酸组氨酸的情况下,其死亡模式与15 TAU菌株相似。在没有组氨酸的情况下,抗生素刺激核糖核酸(RNA)合成,而未检测到对脱氧核糖核酸(DNA)合成的抑制或刺激。在T6r(+)多重感染的条件下,当存在链霉素(40微克/毫升)时,THU的裂解比对照提前1小时发生,产生的DNA和噬菌体约为对照的三分之一。在没有组氨酸从而阻止噬菌体DNA合成的情况下,对照系统和经链霉素处理的系统中病毒诱导的RNA积累在约30分钟内相似。然而,在存在抗生素的情况下,90分钟后感染细胞积累的RNA比对照多约50%至70%。尽管如此,RNA的周转未被链霉素检测到有影响。脱氧胞苷酸羟甲基化酶的产生速率和最终量,以及该酶合成的截止时间,几乎不受链霉素影响。抗生素使DNA合成的开始延迟约3至4分钟。感染细胞中组氨酸的掺入在10分钟内未受影响,在70分钟时仅比对照少约10%。溶菌酶的产生在对照和经抗生素处理的系统中大约在10分钟开始,以基本相似的增加速率持续20分钟,但在经链霉素处理的细胞中尽管蛋白质合成仍在继续却突然停止。除了溶菌酶外,链霉素敏感细菌中噬菌体特异性聚合物的产生仅受到抗生素的轻微影响。