Heude M, Fabre F
Institut Curie-Biologie, Centre Universitaire, Orsay, France.
Genetics. 1993 Mar;133(3):489-98. doi: 10.1093/genetics/133.3.489.
It has long been known that diploid strains of yeast are more resistant to gamma-rays than haploid cells, and that this is in part due to heterozygosity at the mating type (MAT) locus. It is shown here that the genetic control exerted by the MAT genes on DNA repair involves the a1 and alpha 2 genes, in a RME1-independent way. In rad18 diploids, affected in the error-prone repair, the a/alpha effects are of a very large amplitude, after both UV and gamma-rays, and also depends on a1 and alpha 2. The coexpression of a and alpha in rad18 haploids suppresses the sensitivity of a subpopulation corresponding to the G2 phase cells. Related to this, the coexpression of a and alpha in RAD+ haploids depresses UV-induced mutagenesis in G2 cells. For srs2 null diploids, also affected in the error-prone repair pathway, we show that their G1 UV sensitivity, likely due to lethal recombination events, is partly suppressed by MAT homozygosity. Taken together, these results led to the proposal that a1-alpha 2 promotes a channeling of some DNA structures from the mutagenic into the recombinational repair process.
长期以来人们都知道，酵母的二倍体菌株比单倍体细胞对伽马射线更具抗性，部分原因是交配型（MAT）位点的杂合性。本文表明，MAT基因对DNA修复的遗传控制以一种不依赖RME1的方式涉及a1和α2基因。在易错修复受影响的rad18二倍体中，无论是紫外线还是伽马射线照射后，a/α效应的幅度都非常大，并且也依赖于a1和α2。在rad18单倍体中a和α的共表达抑制了与G2期细胞相对应的一个亚群的敏感性。与此相关的是，在RAD+单倍体中a和α的共表达降低了G2细胞中紫外线诱导的诱变。对于同样在易错修复途径中受影响的srs2缺失二倍体，我们表明它们在G1期对紫外线的敏感性（可能是由于致死性重组事件）部分被MAT纯合性所抑制。综上所述，这些结果表明a1-α2促进了一些DNA结构从诱变修复过程导向重组修复过程。
