Moore P D
Mutat Res. 1975 Jun;28(3):355-66. doi: 10.1016/0027-5107(75)90230-4.
The relationship between UV sensitivity and pyrimidine auxotrophy has been examined. Fourteen pyrimidine-requiring mutants have been classified on the basis of genetic complementation and utilization of biosynthetic intermediates and have been assigned to at least four loci. All the mutants studied were sensitive to UV, although the degree of sensitivity varied both between loci and amongst alleles at the same locus. A double mutant strain carrying pyrimidine mutants at two loci was only as sensitive to UV as the more sensitive of the singles. This suggests that both mutants are deficient in the same repair mechanism. Suppressor mutations which restored endogenous pyrimidine biosynthesis were isolated. These suppressors restored UV resistance in the presence of the original mutation. The results indicate that the UV sensitivity of these mutants is a direct result of pyrimidine auxotrophy and not to any secondary properties of the mutants.
紫外线敏感性与嘧啶营养缺陷型之间的关系已得到研究。已根据遗传互补和生物合成中间体的利用情况对14个需要嘧啶的突变体进行了分类，并将它们至少定位到四个基因座。所有研究的突变体对紫外线都敏感，尽管敏感程度在不同基因座之间以及同一基因座的等位基因之间有所不同。在两个基因座携带嘧啶突变体的双突变菌株对紫外线的敏感性仅与较敏感的单突变体相同。这表明这两个突变体在相同的修复机制中存在缺陷。分离出了恢复内源性嘧啶生物合成的抑制突变。这些抑制子在存在原始突变的情况下恢复了紫外线抗性。结果表明，这些突变体对紫外线的敏感性是嘧啶营养缺陷型的直接结果，而不是突变体的任何次要特性所致。
