Siede W, Eckardt F
Gesellschaft für Strahlen- und Umweltforschung, Institut für Strahlenbiologie, Neuherberg, Federal Republic of Germany.
Curr Genet. 1986;10(12):871-8. doi: 10.1007/BF00398283.
A double mutant being thermoconditionally defective in mutation induction as well as in repair of pre-lethal UV-induced DNA damage (rev2ts) and deficient in excision repair (rad3-2) was studied in temperature-shift experiments. The influence of inhibitors of DNA replication (hydroxyurea, aphidicolin) was determined. Additionally, an analysis of the dose-response pattern of mutation induction ("mutation kinetics") at several ochre alleles was carried out. It was concluded that the UV-inducible REV2 dependent mutagenic repair process is not induced in excision-deficient cells. In excision-deficient cells, REV2 dependent mutation fixation is slow and mostly post-replicative though not dependent on DNA replication. The REV2 mediated mutagenic process could be separated from the repair function.
在温度转换实验中研究了一种双突变体,其在突变诱导以及对致死前紫外线诱导的DNA损伤(rev2ts)的修复方面存在温度条件性缺陷,并且在切除修复方面存在缺陷(rad3-2)。确定了DNA复制抑制剂(羟基脲、阿非迪霉素)的影响。此外,还对几个赭石型等位基因的突变诱导剂量反应模式(“突变动力学”)进行了分析。得出的结论是,紫外线诱导的依赖REV2的诱变修复过程在切除缺陷细胞中未被诱导。在切除缺陷细胞中,依赖REV2的突变固定缓慢,且大多是复制后进行的,尽管不依赖于DNA复制。REV2介导的诱变过程可以与修复功能分离。