Doering A M, Jansen M, Cohen S S
J Bacteriol. 1966 Sep;92(3):565-74. doi: 10.1128/jb.92.3.565-574.1966.
Doering, Alice McGovern (University of Pennsylvania School of Medicine, Philadelphia), Miekie Jansen, and Seymour S. Cohen. Polymer synthesis in killed bacteria: lethality of 2',3'-dideoxyadenosine. J. Bacteriol. 92:565-574. 1966.-We studied the metabolic capabilities of cells that had lost the ability to multiply under a variety of lethal treatments. Cultures of a polyauxotrophic mutant of Escherichia coli strain 15 requiring thymine, arginine, uracil, and adenine for growth were killed to a few per cent survivors by several different methods. These treatments included streptomycin, thymineless death, d-arabinosyladenine (ara-A), and 2',3'-dideoxyadenosine (DDA). The killed cells were washed and supplied with complete media, and were compared with control cells with respect to the ability to incorporate thymine, arginine, and uracil. Cells killed with streptomycin in the absence of thymine were only partially inhibited in deoxyribonucleic acid (DNA) synthesis; they were markedly inhibited in synthesis of ribonucleic acid (RNA) and protein. Cells that had suffered thymineless death were essentially uninhibited in DNA synthesis, partially so in RNA synthesis, but extensively inhibited in protein synthesis. Killing by ara-A did not prevent DNA synthesis, but markedly inhibited RNA and protein synthesis. The lethality of DDA was studied in the presence of exogenous adenosine; lethality was partially prevented by deoxyadenosine. Dideoxyadenosine was similar to ara-A and thymineless death in killing in a pattern in which RNA and protein synthesis continued while DNA synthesis was inhibited. Cells killed by DDA, however, were markedly inhibited in subsequent thymine incorporation, unlike cells killed by the other methods. In addition, at this time, the DDA-killed cells were more inhibited in incorporation of arginine than of uracil. DDA also potentiated thymineless death; when cells were killed rapidly by the combined treatment, only the ability to synthesize DNA was lost irreversibly. This agent (DDA) may permit the detailed study in E. coli of the relation of DNA synthesis to numerous phenomena, such as genetic recombination, sequential transcription, and the number and distribution of chromosome breaks.
多林，爱丽丝·麦戈文（宾夕法尼亚大学医学院，费城），米基·扬森，以及西摩·S·科恩。死菌中的聚合物合成：2'，3'-二脱氧腺苷的致死性。《细菌学杂志》92:565 - 574。1966年。——我们研究了在多种致死处理下失去繁殖能力的细胞的代谢能力。一株需要胸腺嘧啶、精氨酸、尿嘧啶和腺嘌呤才能生长的大肠杆菌15多营养缺陷型突变体培养物，通过几种不同方法被杀死至仅百分之几的存活者。这些处理包括链霉素、无胸腺嘧啶死亡、D - 阿拉伯糖基腺嘌呤（ara - A）和2'，3'-二脱氧腺苷（DDA）。将杀死的细胞洗涤后提供完全培养基，并就其掺入胸腺嘧啶、精氨酸和尿嘧啶的能力与对照细胞进行比较。在无胸腺嘧啶的情况下用链霉素杀死的细胞在脱氧核糖核酸（DNA）合成中仅受到部分抑制；它们在核糖核酸（RNA）和蛋白质合成中受到明显抑制。经历无胸腺嘧啶死亡的细胞在DNA合成中基本未受抑制，在RNA合成中部分未受抑制，但在蛋白质合成中受到广泛抑制。ara - A杀死细胞并不阻止DNA合成，但明显抑制RNA和蛋白质合成。在存在外源性腺苷的情况下研究了DDA的致死性；脱氧腺苷可部分阻止致死性。二脱氧腺苷在杀死细胞的模式上与ara - A和无胸腺嘧啶死亡相似，即DNA合成受到抑制时RNA和蛋白质合成仍在继续。然而，与通过其他方法杀死的细胞不同，被DDA杀死的细胞在随后掺入胸腺嘧啶方面受到明显抑制。此外，此时，被DDA杀死的细胞在掺入精氨酸方面比掺入尿嘧啶受到的抑制更明显。DDA还增强了无胸腺嘧啶死亡；当细胞通过联合处理快速被杀死时，只有合成DNA的能力被不可逆地丧失。这种试剂（DDA）可能有助于在大肠杆菌中详细研究DNA合成与众多现象的关系，如基因重组、顺序转录以及染色体断裂的数量和分布。
