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首页> 外文OA文献 >Recognition and repair of compound DNA lesions (base damage and mismatch) by human mismatch repair and excision repair systems.
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Recognition and repair of compound DNA lesions (base damage and mismatch) by human mismatch repair and excision repair systems.

机译：通过人类错配修复和切除修复系统识别和修复复合DNA损伤（碱基损伤和错配）。

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摘要

Nucleotide excision repair and the long-patch mismatch repair systems correct abnormal DNA structures arising from DNA damage and replication errors, respectively. DNA synthesis past a damaged base (translesion replication) often causes misincorporation at the lesion site. In addition, mismatches are hot spots for DNA damage because of increased susceptibility of unpaired bases to chemical modification. We call such a DNA lesion, that is, a base damage superimposed on a mismatch, a compound lesion. To learn about the processing of compound lesions by human cells, synthetic compound lesions containing UV photoproducts or cisplatin 1,2-d(GpG) intrastrand cross-link and mismatch were tested for binding to the human mismatch recognition complex hMutS alpha and for excision by the human excision nuclease. No functional overlap between excision repair and mismatch repair was observed. The presence of a thymine dimer or a cisplatin diadduct in the context of a G-T mismatch reduced the affinity of hMutS alpha for the mismatch. In contrast, the damaged bases in these compound lesions were excised three- to fourfold faster than simple lesions by the human excision nuclease, regardless of the presence of hMutS alpha in the reaction. These results provide a new perspective on how excision repair, a cellular defense system for maintaining genomic integrity, can fix mutations under certain circumstances.
机译：核苷酸切除修复和长补丁错配修复系统分别纠正了DNA损伤和复制错误引起的异常DNA结构。超过受损碱基的DNA合成（病灶复制）通常会在病灶部位引起错误掺入。此外，由于未配对碱基对化学修饰的敏感性增加，错配是DNA损伤的热点。我们将这种DNA损伤称为复合损伤，将基础损伤叠加在错配上。为了了解人类细胞对复合损伤的处理，测试了含有紫外线光产物或顺铂1,2-d（GpG）链内交联和错配的合成复合损伤与人错配识别复合体hMutS alpha的结合力以及通过人类切除核酸酶。切除修复和错配修复之间未发现功能重叠。在G-T错配的情况下胸腺嘧啶二聚体或顺铂二加合物的存在降低了hMutS alpha对错配的亲和力。相反，无论反应中是否存在hMutS alpha，人类切除核酸酶均能将这些复合病变中受损碱基的切除速度比简单病变快三至四倍。这些结果为切除修复（一种用于维持基因组完整性的细胞防御系统）如何在某些情况下修复突变提供了新的视角。

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