Montelone B A, Liang-Chong B C
Division of Biology, Kansas State University, Manhattan 66506.
Curr Genet. 1993 Dec;24(6):481-6. doi: 10.1007/BF00351709.
We have tested the ability of mutants of three additional genes in the excision repair pathway of Saccharomyces cerevisiae to suppress the hyper-recombination and rad52 double-mutant lethality phenotypes of the rad3-102 (formerly rem1-2) mutation. Such suppression has previously been observed with mutant alleles of RAD1 and RAD4. We had hypothesized that the rad3-102 mutation created elevated levels of DNA lesions which could be processed by the products of the RAD1 and RAD4 genes into recombinogenic double-strand breaks requiring the RAD52 product for repair. In this report, we show that the RAD2, RAD7, and RAD10 genes are also necessary for this processing. We discuss our observations of varying levels of mitotic crossing-over in Rem- rad double-mutant strains.
我们测试了酿酒酵母切除修复途径中另外三个基因的突变体抑制rad3-102（以前称为rem1-2）突变的高重组和rad52双突变致死表型的能力。此前已观察到RAD1和RAD4的突变等位基因具有这种抑制作用。我们曾假设，rad3-102突变会导致DNA损伤水平升高，而RAD1和RAD4基因的产物可将这些损伤加工成需要RAD52产物进行修复的重组双链断裂。在本报告中，我们表明RAD2、RAD7和RAD10基因对于这种加工也是必需的。我们讨论了在Rem-rad双突变菌株中观察到的不同水平的有丝分裂交换。
