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首页> 外文期刊>Molecular and Cellular Biology >Pyrimidine dimers block simian virus 40 replication forks.
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Pyrimidine dimers block simian virus 40 replication forks.

机译：嘧啶二聚体阻断猿猴病毒40个复制叉。

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摘要

UV light produces lesions, predominantly pyrimidine dimers, which inhibit DNA replication in mammalian cells. The mechanism of inhibition is controversial: is synthesis of a daughter strand halted at a lesion while the replication fork moves on and reinitiates downstream, or is fork progression itself blocked for some time at the site of a lesion? We directly addressed this question by using electron microscopy to examine the distances of replication forks from the origin in unirradiated and UV-irradiated simian virus 40 chromosomes. If UV lesions block replication fork progression, the forks should be asymmetrically located in a large fraction of the irradiated molecules; if replication forks move rapidly past lesions, the forks should be symmetrically located. A large fraction of the simian virus 40 replication forks in irradiated molecules were asymmetrically located, demonstrating that UV lesions present at the frequency of pyrimidine dimers block replication forks. As a mechanism for this fork blockage, we propose that polymerization of the leading strand makes a significant contribution to the energetics of fork movement, so any lesion in the template for the leading strand which blocks polymerization should also block fork movement.
机译：紫外线会产生损伤，主要是嘧啶二聚体，从而抑制哺乳动物细胞中DNA的复制。抑制的机制是有争议的：在复制叉继续前进并向下游重新启动时，病变处的子链合成停止了吗，还是叉前进本身在病变部位被阻止了一段时间？我们通过使用电子显微镜检查复制叉到未经辐照和紫外线辐照的猿猴病毒40染色体中的起点的距离，直接解决了这个问题。如果紫外线损伤阻止了复制叉的前进，则叉应不对称地位于大部分受辐照分子中;如果复制叉快速移过病变，则叉应对称放置。辐照过的猿猴病毒40个复制叉中有很大一部分位于不对称位置，这表明以嘧啶二聚体的频率存在的紫外线损伤会阻止复制叉。作为这种叉子阻塞的机制，我们建议前导链的聚合对前叉运动的能量有重要贡献，因此前导链模板中任何阻止聚合的病变也应阻止前叉运动。

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