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首页> 外文期刊>Nucleic Acids Research >Delayed DNA joining at 3' mismatches by human DNA ligases.
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Delayed DNA joining at 3' mismatches by human DNA ligases.

机译：人DNA连接酶在3'错配处延迟的DNA连接。

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摘要

Repair synthesis catalysed by DNA polymerase beta at 1 nt gaps occurs in the main pathway of mammalian base excision repair. DNA polymerase beta has no exonucleolytic proof-reading ability, and exhibits high error frequency during DNA synthesis. Consequently, continuous correction of endogenous DNA damage by short-patch repair synthesis might lead to a high spontaneous mutation rate, unless subsequent steps in the repair pathway allow for selective removal of incorporation errors. We show here that both human DNA ligase I and III discriminate strongly between a correctly paired versus a mispaired residue at the 3' position of a nick in DNA, when assayed in the presence of physiological concentrations of KCl. The resulting delay in joining after misincorporation by DNA polymerase beta during gap filling could allow for removal of the mismatched terminal residue by a distinct 3' exonuclease.
机译：DNA聚合酶β在1 nt的缺口处催化的修复合成发生在哺乳动物碱基切除修复的主要途径中。 DNA聚合酶β没有核酸外切的校对能力，在DNA合成过程中出现高错误频率。因此，除非修补途径中的后续步骤允许选择性消除掺入错误，否则通过短修补修复合成对内源性DNA损伤的连续校正可能会导致高自发突变率。我们在这里显示，当在生理浓度的KCl存在下进行测定时，人类DNA连接酶I和III在DNA刻痕的3'位置的正确配对残基与配对残基之间存在强烈区别。在间隙填充过程中，DNA聚合酶β错掺入后所导致的连接延迟可以允许通过独特的3'外切核酸酶去除错配的末端残基。

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