Brychcy T, Von Borstel R C
Mutat Res. 1977 Nov;45(2):185-94. doi: 10.1016/0027-5107(77)90018-5.
The genes RAD1, RAD2, RAD3 and RAD4 encode enzymes in the pathway leading to excision repair of UV-induced DNA damage in Saccharomyces cerevisiae. Four mutant alleles of these loci (rad1-1, rad2-2, rad3-12, and rad4-3) were studied for their effect on spontaneous reversion rate to lysine and histidine independence, by means of the 1000-compartment fluctuation test of von Borstel, Cain and Steinberg. Of these four excision-defective alleles, only rad3-12 was found to substantially increase the spontaneous reversion rate of the nonsense-suppressible lys1-1 allele, both through locus reversion as well as by forward mutation at one of eight suppressor loci. Similarly, only rad3-12 conferred a considerable increase in the reversion frequency of the missense his1-7 mutant. As the RAD3 gene product is believed to mediate the first step in the excision-repair pathway, it is assumed that spontaneous lesions in the rad3 strain are channelled into a mutagenic repair pathway, thus accounting for the enhanced spontaneous mutation rate.
基因RAD1、RAD2、RAD3和RAD4编码酿酒酵母中紫外线诱导的DNA损伤切除修复途径中的酶。通过冯·博斯特尔、凯恩和斯坦伯格的1000室波动试验，研究了这些基因座的四个突变等位基因（rad1-1、rad2-2、rad3-12和rad4-3）对赖氨酸和组氨酸非依赖型自发回复突变率的影响。在这四个切除缺陷等位基因中，仅发现rad3-12通过基因座回复突变以及八个抑制基因座之一的正向突变，大幅提高了无义抑制型lys1-1等位基因的自发回复突变率。同样，只有rad3-12使错义his1-7突变体的回复突变频率大幅增加。由于RAD3基因产物被认为介导切除修复途径的第一步，因此推测rad3菌株中的自发损伤被导向诱变修复途径，从而解释了自发突变率的提高。
