Bohr V A, Smith C A, Okumoto D S, Hanawalt P C
Cell. 1985 Feb;40(2):359-69. doi: 10.1016/0092-8674(85)90150-3.
DNA repair was measured in the dihydrofolate reductase gene in Chinese hamster ovary cells, amplified for the gene, by quantitating pyrimidine dimers with a specific UV-endonuclease. More than two thirds of the dimers had been removed from a 14.1 kb restriction fragment of the gene by 26 hr after irradiation (20 J/m2), while little removal was detected in fragments upstream of the gene and only 15% were removed from the genome overall. This suggests that damage processing can vary according to function or activity of affected sequences, which has general implications for correlations of DNA repair with survival and mutagenesis. Perhaps preferential repair of vital sequences facilitates UV-resistance of these cells despite low overall repair levels.
通过用一种特异性紫外线内切酶定量嘧啶二聚体,在中国仓鼠卵巢细胞中测量二氢叶酸还原酶基因的DNA修复情况,该基因已被扩增。照射(20 J/m²)后26小时,超过三分之二的二聚体已从该基因的一个14.1 kb限制性片段中去除,而在该基因上游的片段中几乎没有检测到去除情况,总体上从基因组中仅去除了15%。这表明损伤处理可能会根据受影响序列的功能或活性而有所不同,这对于DNA修复与存活及诱变之间的相关性具有普遍意义。尽管总体修复水平较低,但重要序列的优先修复可能有助于这些细胞的抗紫外线能力。