Inactivation of Escherichia coli, F′ Episomes at Transfer, and Bacteriophage Lambda by Psoralen Plus 360-nm Light: Significance of Deoxyribonucleic Acid Cross-Links
Inactivation of Escherichia coli, F′ Episomes at Transfer, and Bacteriophage Lambda by Psoralen Plus 360-nm Light: Significance of Deoxyribonucleic Acid Cross-Links
复制标题
补骨脂素加上 360 nm 光灭活大肠杆菌、转移时的 F 游离体和噬菌体 Lambda：脱氧核糖核酸交联的意义
作者：
R. S. Cole
我们研究了光诱导的补骨脂素-脱氧核糖核酸（DNA）加合物的一些生物学后果，发现对于大肠杆菌的几种功能（杀死菌株AB2480 recA13 uvrA6，在野生型和uvrA6宿主中噬菌体lambda斑块形成能力失活，丧失传播完整Flac+片段的能力），足以产生每个DNA分子单个交联的光暴露与生物学后果密切相关。虽然每个基因组一个交联对recA13 uvr -菌株显然是致命的，但携带recA13或uvrA6标记的突变体在光照下存活下来，每个基因组分别产生6.7和16个交联，野生型细胞从65个补骨脂素交联中恢复过来。显然，在从含有补骨脂素光产物的细胞DNA中重建完整基因组时，切除和重组修复系统是相互补充的。上述细菌和噬菌体菌株，DNA修复过程最小化，对嘧啶二聚体形成的254 nm紫外光（不含补骨脂素）也非常敏感，并且预计对其DNA中补骨脂素-嘧啶基单加合物的形成也有类似的反应。由于补骨脂素的生物失活与交联的形成密切相关，我们认为这种药物的增敏作用主要来自于它形成DNA交联的能力。
We have investigated some biological consequences of light-induced psoralen-deoxyribonucleic acid (DNA) adducts and find that for several Escherichia coli functions (killing of strain AB2480 recA13 uvrA6, inactivation of phage lambda plaque-forming ability in wild type and uvrA6 hosts, loss of ability to transmit intact Flac+ episomes), a light exposure sufficient for production of a single cross-link per DNA molecule correlates well with the biological consequence. Although one cross-link per genome is apparently lethal to recA13 uvr− strains, mutants carrying the recA13 or uvrA6 markers survive light exposures producing 6.7 and 16 cross-links per genome, respectively, and wild-type cells recover from 65 psoralen cross-links. Evidently, the excision and recombinational repair systems complement one another in reconstructing an intact genome from cellular DNA containing psoralen photoproducts. The above bacterial and phage strains, in which DNA repair processes are minimized, are also extremely sensitive to pyrimidine dimer-forming 254-nm UV light (without psoralen), and were expected to respond similarly to formation of psoralen-pyrimidine base monoadducts in their DNA. Since the biological inactivation by psoralen correlates well with cross-link formation, we suggest that the sensitizing action of this drug primarily derives from its ability to form DNA cross-links.