Ganesan A K, Hanawalt P C
Department of Biological Sciences, Stanford University, California 94305-5020.
Somat Cell Mol Genet. 1994 May;20(3):233-42. doi: 10.1007/BF02254762.
A shuttle vector (pZH-1) carrying the E. coli lacZ gene under control of the SV40 early promoter was irradiated with UV and introduced into repair-proficient or repair-deficient human cell lines. The expression of irradiated lacZ compared to unirradiated lacZ was greater in repair-proficient cells (HT-1080) than in repair-deficient cells (XP12RO-SV40) belonging to xeroderma pigmentosum complementation group A. To ascertain whether the expression of lacZ in the repair-proficient cells was correlated with the removal of cyclobutane pyrimidine dimers (CPDs), we purified DNA from the recipient cells and used the CPD-specific enzyme T4 endonuclease V to measure the frequency of CPDs remaining in the plasmid as a whole and in two restriction fragments derived from it. We found that removal of CPDs occurred in both fragments in the repair-proficient cells but not in the repair-deficient cells. Our results provide the first direct evidence for the removal of CPDs from UV irradiated plasmids introduced into human cells and support the notion that expression of the UV-damaged lacZ gene in repair-proficient human cells reflects the removal of transcription blocking lesions from the gene.
一种携带在SV40早期启动子控制下的大肠杆菌lacZ基因的穿梭载体(pZH - 1)经紫外线照射后,被导入具有修复能力或修复缺陷的人类细胞系。与未照射的lacZ相比,照射后的lacZ在具有修复能力的细胞(HT - 1080)中的表达高于属于色素性干皮病A互补组的修复缺陷细胞(XP12RO - SV40)。为了确定具有修复能力的细胞中lacZ的表达是否与环丁烷嘧啶二聚体(CPD)的去除相关,我们从受体细胞中纯化DNA,并使用CPD特异性酶T4内切核酸酶V来测量整个质粒以及由其衍生的两个限制性片段中剩余CPD的频率。我们发现,具有修复能力的细胞中两个片段的CPD都被去除了,而修复缺陷细胞中则没有。我们的结果为从导入人类细胞的紫外线照射质粒中去除CPD提供了首个直接证据,并支持这样一种观点,即紫外线损伤的lacZ基因在具有修复能力的人类细胞中的表达反映了该基因转录阻断损伤的去除。