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首页> 外文期刊>Molecular and Cellular Biology >Xeroderma pigmentosum complementation group C cells remove pyrimidine dimers selectively from the transcribed strand of active genes.
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Xeroderma pigmentosum complementation group C cells remove pyrimidine dimers selectively from the transcribed strand of active genes.

机译：色皮干燥菌互补组C细胞选择性地从转录的活性基因链中去除嘧啶二聚体。

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摘要

We have measured the removal of UV-induced pyrimidine dimers from DNA fragments of the adenosine deaminase (ADA) and dihydrofolate reductase (DHFR) genes in primary normal human and xeroderma pigmentosum complementation group C (XP-C) cells. Using strand-specific probes, we show that in normal cells, preferential repair of the 5' part of the ADA gene is due to the rapid and efficient repair of the transcribed strand. Within 8 h after irradiation with UV at 10 J m-2, 70% of the pyrimidine dimers in this strand are removed. The nontranscribed strand is repaired at a much slower rate, with 30% dimers removed after 8 h. Repair of the transcribed strand in XP-C cells occurs at a rate indistinguishable from that in normal cells, but the nontranscribed strand is not repaired significantly in these cells. Similar results were obtained for the DHFR gene. In the 3' part of the ADA gene, however, both normal and XP-C cells perform fast and efficient repair of either strand, which is likely to be caused by the presence of transcription units on both strands. The factor defective in XP-C cells is apparently involved in the processing of DNA damage in inactive parts of the genome, including nontranscribed strands of active genes. These findings have important implications for the understanding of the mechanism of UV-induced excision repair and mutagenesis in mammalian cells.
机译：我们测量了原代正常人和干性色素干性补充C组（XP-C）细胞中腺苷脱氨酶（ADA）和二氢叶酸还原酶（DHFR）基因的DNA片段中UV诱导的嘧啶二聚体的去除。使用链特异性探针，我们显示在正常细胞中，ADA基因5'部分的优先修复是由于转录链的快速有效修复。在10 J m-2的紫外线照射后8小时内，该链中70％的嘧啶二聚体被去除。非转录链的修复速度要慢得多，8小时后去除了30％的二聚体。 XP-C细胞中转录链的修复发生率与正常细胞中没有区别，但未转录的链在这些细胞中未得到明显修复。 DHFR基因获得了相似的结果。但是，在ADA基因的3'部分中，正常细胞和XP-C细胞均对任一条链进行了快速有效的修复，这很可能是由于两条链上都存在转录单元所致。 XP-C细胞中的缺陷因子显然参与了基因组非活性部分（包括活性基因的非转录链）DNA损伤的处理。这些发现对于理解紫外线诱导的哺乳动物细胞中的切除修复和诱变的机制具有重要意义。

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