Schiestl R H, Prakash S, Prakash L
Department of Biology, University of Rochester, New York 14627.
Genetics. 1990 Apr;124(4):817-31. doi: 10.1093/genetics/124.4.817.
rad6 mutants of Saccharomyces cerevisiae are defective in the repair of damaged DNA, DNA damage induced mutagenesis, and sporulation. In order to identify genes that can substitute for RAD6 function, we have isolated genomic suppressors of the UV sensitivity of rad6 deletion (rad6 delta) mutations and show that they also suppress the gamma-ray sensitivity but not the UV mutagenesis or sporulation defects of rad6. The suppressors show semidominance for suppression of UV sensitivity and dominance for suppression of gamma-ray sensitivity. The six suppressor mutations we isolated are all alleles of the same locus and are also allelic to a previously described suppressor of the rad6-1 nonsense mutation, SRS2. We show that suppression of rad6 delta is dependent on the RAD52 recombinational repair pathway since suppression is not observed in the rad6 delta SRS2 strain containing an additional mutation in either the RAD51, RAD52, RAD54, RAD55 or RAD57 genes. Possible mechanisms by which SRS2 may channel unrepaired DNA lesions into the RAD52 DNA repair pathway are discussed.
酿酒酵母的rad6突变体在受损DNA修复、DNA损伤诱导的诱变和孢子形成方面存在缺陷。为了鉴定能够替代RAD6功能的基因,我们分离出了rad6缺失(rad6δ)突变的紫外线敏感性的基因组抑制子,并表明它们也能抑制γ射线敏感性,但不能抑制rad6的紫外线诱变或孢子形成缺陷。这些抑制子在抑制紫外线敏感性方面表现出半显性,在抑制γ射线敏感性方面表现出显性。我们分离出的六个抑制子突变都是同一基因座的等位基因,并且也与先前描述的rad6-1无义突变的抑制子SRS2等位。我们表明,rad6δ的抑制依赖于RAD52重组修复途径,因为在rad6δSRS2菌株中,若RAD51、RAD52、RAD54、RAD55或RAD57基因发生额外突变,则不会观察到抑制现象。文中讨论了SRS2可能将未修复的DNA损伤导入RAD52 DNA修复途径的潜在机制。