de Cock J G, Klink E C, Ferro W, Lohman P H, Eeken J C
MGC-Department of Radiation Genetics and Chemical Mutagenesis, State University of Leiden, Netherlands.
Mutat Res. 1992 Nov;293(1):11-20. doi: 10.1016/0921-8777(92)90003-l.
Nucleotide excision repair (NER) of ultraviolet (UV) light induced cyclobutane pyrimidine dimers (CPDs) was assayed in a Drosophila melanogaster Kc subline that responds to treatment with the steroid hormone 20-hydroxyecdysone (20-OH-E; beta-ecdysone, ecdysterone). In this cell line the hormone induces transcription of the beta 3-tubulin gene which is not expressed under standard culture conditions. Cells were exposed to either 10 or 15 J/m2 UV (predominantly 254-nm) and removal of CPDs from several genes, including beta 3-tubulin, and total cellular DNA was assayed. We show that upon induction of transcription of the beta 3-tubulin gene, its repair is not enhanced. In non-treated as well as 20-OH-E treated cells, repair kinetics in beta 3-tubulin resemble those in the active genes Gart and Notch, the inactive locus white and total cellular DNA. Moreover, in the presence as well as in the absence of transcription, the separate strands of the beta 3-tubulin gene are repaired with the same rate and to the same extent: about 90% after 24 h. It can be concluded from these observations that transcription is not a prerequisite for the efficient repair of CPDs in the Drosophila embryonic Kc cell line.
在一种对类固醇激素20-羟基蜕皮激素（20-OH-E；β-蜕皮激素、蜕皮甾酮）处理有反应的黑腹果蝇Kc亚系中，检测了紫外线（UV）诱导的环丁烷嘧啶二聚体（CPD）的核苷酸切除修复（NER）。在这种细胞系中，该激素可诱导β3-微管蛋白基因的转录，而该基因在标准培养条件下不表达。将细胞暴露于10或15 J/m2的紫外线（主要是254 nm）下，检测包括β3-微管蛋白在内的多个基因以及总细胞DNA中CPD的去除情况。我们发现，在诱导β3-微管蛋白基因转录后，其修复并未增强。在未处理以及经20-OH-E处理的细胞中，β3-微管蛋白的修复动力学与活性基因Gart和Notch、非活性位点white以及总细胞DNA中的相似。此外，无论有无转录，β3-微管蛋白基因的单链修复速率和程度相同：24小时后约为90%。从这些观察结果可以得出结论，转录不是黑腹果蝇胚胎Kc细胞系中CPD高效修复的先决条件。
