McKee R H, Lawrence C W
Genetics. 1979 Oct;93(2):361-73. doi: 10.1093/genetics/93.2.361.
The frequency of revertants induced by 60Co gamma rays of the ochre allele, cyc1-9, has been measured in radiation-sensitive strains carrying one of 19 nonallelic mutations and in wild-type strains. The results indicate that ionizing radiation mutagenesis depends on the activity of the RAD6 group of genes and that the gene functions employed are very similar, but probably not identical, to those that mediate UV mutagenesis. Repair activities dependent on the functions of the RAD50 through RAD57 loci, the major pathway for the repair of damage caused by ionizing radiation, do not appear to play any part in mutagenesis. A comparison between the gamma-ray data and those obtained previously with UV (LAWRENCE and CHRISTENSEN 1976) and chemical mutagens (PRAKASH 1976) suggests that the RAD6 "mutagenic pathway" is in fact composed of a set of processes, some of which are concerned with error-prone, and some with error-free, recovery activities.
已在携带19种非等位基因突变之一的辐射敏感菌株和野生型菌株中,测定了60Coγ射线诱导赭石型等位基因cyc1-9回复体的频率。结果表明,电离辐射诱变取决于RAD6基因群的活性,且所利用的基因功能与介导紫外线诱变的基因功能非常相似,但可能并不完全相同。依赖于RAD50至RAD57位点功能的修复活性,即电离辐射所致损伤修复的主要途径,似乎在诱变过程中不起任何作用。γ射线数据与先前用紫外线(劳伦斯和克里斯蒂安森,1976年)及化学诱变剂(普拉卡什,1976年)所获得的数据之间的比较表明,RAD6“诱变途径”实际上由一组过程组成,其中一些过程与易出错的恢复活性有关,而另一些则与无差错的恢复活性有关。