Filippov V D, Lotareva O V
Genetika. 1990 Sep;26(9):1679-81.
In E. coli WP2 trpE65 cells irradiated with UV-dose of 11 J/m2, the additional small portion of induced Trp+ mutations became resistant to photoreactivation or "dark" (excision) repair after a short-termed (10-30 min) postirradiation incubation of bacteria in a minimal medium deprived of glucose and tryptophan. Since protein synthesis could not proceed in those cells because of the lack of energy and tryptophan, the data indicate that an unknown mechanism exists which imparts some mutations with the resistance to antimutagenic repair in the absence of the inducible mutagenic system. In the light of this result, one could suggest that the normal process of mutation fixation (that is the loss of sensitivity of mutations to photoreactivation or to excision repair in cells incubated in growth medium after irradiation) should not necessarily be a direct consequence of manifestation of the activity of an inducible mutagenic system.
在用11 J/m²紫外线剂量照射的大肠杆菌WP2 trpE65细胞中,在缺乏葡萄糖和色氨酸的基本培养基中对细菌进行短期(10 - 30分钟)照射后培养,诱导产生的一小部分Trp⁺突变对光复活或“暗”(切除)修复产生抗性。由于这些细胞因缺乏能量和色氨酸而无法进行蛋白质合成,数据表明存在一种未知机制,在没有可诱导诱变系统的情况下,赋予某些突变对抗诱变修复的抗性。鉴于这一结果,可以认为突变固定的正常过程(即照射后在生长培养基中培养的细胞中突变对光复活或切除修复的敏感性丧失)不一定是可诱导诱变系统活性表现的直接结果。