Ishizaki K, Nishizawa K, Mimaki S, Aizawa S
Laboratory of Experimental Radiology, Aichi Cancer Center Research Institute, Nagoya, Japan.
Mutat Res. 1996 Sep 2;364(1):43-9. doi: 10.1016/0921-8777(96)00020-1.
To verify the genetic instability of p53-deficient cells, UV-induced mutation of the supF gene on a shuttle vector was analyzed. UV-irradiated or non-irradiated shuttle vector plasmid carrying the supF gene as a target of mutation (pYZ289) was introduced into p53-deficient and p53-proficient mouse embryonic fibroblasts, and then the plasmid DNA replicated in mouse cells was recovered. Survival of UV-irradiated plasmid was almost equivalent in both p53-deficient and p53-proficient cells. The frequencies of UV-induced mutation of the supF gene were also the same in both types of cells. However, the distributions of base change mutations in the supF sequence were different between p53-deficient and p53-proficient cells; especially the locations of tandem CpC to TpT changes exhibited a marked difference. Since DNA repair activities of these two types of cell were almost the same, these qualitative differences in UV-induced mutations were probably caused by as yet unidentified differences in other than DNA repair activity.
为验证p53缺陷细胞的基因不稳定性,分析了穿梭载体上紫外线诱导的supF基因突变。将携带作为突变靶点的supF基因的紫外线照射或未照射的穿梭载体质粒(pYZ289)导入p53缺陷型和p53正常型小鼠胚胎成纤维细胞,然后回收在小鼠细胞中复制的质粒DNA。紫外线照射质粒在p53缺陷型和p53正常型细胞中的存活率几乎相同。两种类型细胞中紫外线诱导的supF基因突变频率也相同。然而,p53缺陷型和p53正常型细胞中supF序列碱基变化突变的分布不同;特别是串联CpC到TpT变化的位置表现出明显差异。由于这两种类型细胞的DNA修复活性几乎相同,紫外线诱导突变的这些定性差异可能是由DNA修复活性以外尚未确定的差异引起的。