McKee R H, Lawrence C W
Mutat Res. 1980 Mar;70(1):37-48. doi: 10.1016/0027-5107(80)90056-1.
Comparisons between the 60Co gamma-ray survival curves of diploid strains of the yeast Saccharomyces cerevisiae that are homozygous for two non-allelic radiation-sensitive mutations and the corresponding single-mutant diploids suggest that there are two main types of repair of ionizing radiation damage in this organism. The first, which is defined by the rad52 epistasis group, depends on the activities of the RAD50 through RAD57 genes and is responsible for repairing the larger amount of lethal damage. Previous work [22] shows that this type of repair is essentially error-free. The second, defined by the rad6 epistasis group, depends on the activities of the RAD6, RAD9, RAD18, REV1 and REV3 genes and repairs a smaller, though still substantial, amount of lethal damage. It is also responsible for induced mutagenesis [22, 23]. Data for survival and mutation induction after irradiation in air and partial anoxia show that oxygen-dependent damage can be repaired by either of these two pathways. They also show similar oxygen-enhancement ratios for survival and mutagenesis.
对酿酒酵母二倍体菌株的(^{60}Co)γ射线存活曲线进行比较,这些菌株对于两个非等位辐射敏感突变是纯合的,与相应的单突变二倍体相比,表明该生物体中存在两种主要的电离辐射损伤修复类型。第一种由rad52上位性群定义,依赖于RAD50至RAD57基因的活性,负责修复大量的致死损伤。先前的工作[22]表明,这种修复类型基本上是无差错的。第二种由rad6上位性群定义,依赖于RAD6、RAD9、RAD18、REV1和REV3基因的活性,修复较少量但仍然可观的致死损伤。它还负责诱导诱变[22,23]。在空气和部分缺氧条件下辐照后的存活和突变诱导数据表明,氧依赖性损伤可以通过这两种途径中的任何一种进行修复。它们在存活和诱变方面也显示出相似的氧增强比。