Filippov V D, El-Halfawy K A
Mutat Res. 1981 Jul;82(2):251-61. doi: 10.1016/0027-5107(81)90154-8.
The influence was studied of a temporary specific inhibition of post-radiation macromolecular synthesis and of preliminary UV irradiation on the kinetics of accumulation of fixed mutations, that is mutations insensitive to MFD, in UV-irradiated B. subtilis cells. From experimental results it is deduced that the entry of a pre-mutagenic lesion into a round of replication, initiated before irradiation, is not a fixing event in UV mutagenesis. For performance of fixation, the proceeding of replication, initiated after irradiation, and protein synthesis are necessary. In irradiated cells incubated in medium with lowered concentration of nitrogen sources, the antimutagenic activity of a uvr+-dependent repair system competes with the process of fixation for pre-mutagenic lesions and reduces the efficiency of mutagenesis. The most efficient fixation and mutagenesis occur at high concentrations of nitrogen sources in post-radiation medium, when the manifestation of antimutagenic activity appears to be blocked. The possible nature of a process leading to mutation fixation is discussed.
研究了对辐射后大分子合成的暂时特异性抑制以及预先紫外线照射对紫外线照射的枯草芽孢杆菌细胞中固定突变（即对多因子灭活不敏感的突变）积累动力学的影响。从实验结果推断，诱变前损伤进入照射前启动的一轮复制中，并非紫外线诱变中的固定事件。为了实现固定，照射后启动的复制过程和蛋白质合成是必需的。在氮源浓度降低的培养基中培养的照射细胞中，uvr⁺依赖性修复系统的抗诱变活性与诱变前损伤的固定过程相互竞争，并降低了诱变效率。当抗诱变活性的表现似乎被阻断时，在辐射后培养基中高浓度氮源条件下会发生最有效的固定和诱变。文中讨论了导致突变固定过程的可能性质。
