Kozhina T N, Korolev V G
Genetika. 2012 Apr;48(4):551-5.
Within eukaryotes, tolerance to DNA damage is determined primarily by the repair pathway controlled by the members of the RAD6 epistasis group. Genetic studies on a yeast Saccharomyces cerevisiae model showed that the initial stage of postreplication repair (PRR), i.e., initiation of replication through DNA damage, is controlled by Rad6-Rad18 ubiquitin-conjugating enzyme complex. Mutants of these genes are highly sensitive to various genotoxic agents and reduce the level of induced mutagenesis. In this case, the efficiency of mutagenesis suppression depends on the type of damage. In this study we showed that DNA damage induced by hydrogen peroxide at the same mutagen doses causes significantly more mutations and lethal events in the rad18 mutant cells compared to control wild-type cells.
在真核生物中，对DNA损伤的耐受性主要由RAD6上位性基因组成员控制的修复途径决定。对酵母酿酒酵母模型的遗传学研究表明，复制后修复（PRR）的初始阶段，即通过DNA损伤启动复制，由Rad6-Rad18泛素结合酶复合物控制。这些基因的突变体对各种基因毒性剂高度敏感，并降低诱导诱变的水平。在这种情况下，诱变抑制的效率取决于损伤的类型。在本研究中，我们表明，与对照野生型细胞相比，在相同诱变剂量下，过氧化氢诱导的DNA损伤在rad18突变体细胞中导致更多的突变和致死事件。
