INDUCTION OF THE ESCHERICHIA-COLI LACTOSE OPERON SELECTIVELY INCREASES REPAIR OF ITS TRANSCRIBED DNA STRAND
INDUCTION OF THE ESCHERICHIA-COLI LACTOSE OPERON SELECTIVELY INCREASES REPAIR OF ITS TRANSCRIBED DNA STRAND
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DOI：
10.1038/342095a0
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发表时间：
1989-11-02
期刊：
影响因子：
64.8
通讯作者：
HANAWALT, PC
中科院分区：
文献类型：
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作者：
MELLON, I;HANAWALT, PC
核苷酸切除修复通过从细胞基因组中去除螺旋扭曲损伤，有助于改善 DNA 损伤的致命和诱变后果1。我们之前分析了哺乳动物细胞中紫外线诱导的环丁烷嘧啶二聚体从特定 DNA 序列中的去除，并证明转录活性基因优先修复2-4。此外，我们发现在啮齿动物和人类细胞中，只有二氢叶酸还原酶基因的转录链被选择性修复5。转录被模板 DNA 中的嘧啶二聚体阻断，选择性去除这些损伤似乎对于紫外线照射后细胞的存活很重要2,7,8。为了确定这种修复特征是否为原核生物和真核生物所共有，并更好地理解其机制，我们研究了紫外线照射的大肠杆菌乳糖操纵子的两条独立DNA链的修复。我们发现，只有当转录被诱导时，两条链的修复才会出现显着差异。大多数二聚体在照射后五分钟内从诱导操纵子的转录链中去除。在非转录链中，修复速度明显较慢，与非诱导操纵子两条链中的修复类似。因此，似乎存在一种将核苷酸切除修复和转录结合起来的机制。
NUCLEOTIDE excision repair helps to ameliorate the lethal and mutagenic consequences of DNA damage by removing helix-distorting lesions from cellular genomes1. We have pre-viously analysed the removal of ultraviolet-induced cyclobutane pyrimidine dimers from specific DNA sequences in mammalian cells and demonstrated that transcriptionally active genes are preferentially repaired2–4. Additionally, we found that in rodent and human cells only the transcribed strand of the dihydrofolate reductase gene is selectively repaired5. Transcription is blocked by pyrimidine dimers in template DNA6and the selective removal of these lesions seems to be important for cell survival after irradiation with ultraviolet light2,7,8. To determine whether this feature of repair is common to prokaryotes and eukaryotes and better to understand its mechanism, we have investigated repair in the two separate DNA strands of the lactose operon of ultraviolet-irradiatedEscherichia coli. We find a dramatic difference in the repair of the two strands only when transcription is induced. Most dimers are removed from the transcribed strand of the induced operon within five minutes of irradiation. In the non-transcribed strand, repair is significantly slower and resembles that found in both strands of the uninduced operon. Thus there seems to be a mechanism that couples nucleotide excision repair and transcription.