Institute of Chemical Biology and Fundamental Medicine, Siberian Branch, Russian Academy of Sciences, Novosibirsk, Russia.
Novosibirsk State University, Novosibirsk, Russia.
Dokl Biochem Biophys. 2023 Dec;513(Suppl 1):S82-S86. doi: 10.1134/S1607672923600355. Epub 2024 Feb 9.
The presence of DNA damage can increase the likelihood of DNA replication errors and promote mutations. In particular, pauses of DNA polymerase at the site of damage can lead to polymerase slippage and the formation of 1-2-nucleotide bulges. Repair of such structures using an undamaged DNA template leads to small deletions. One of the most abundant oxidative DNA lesions, 8-oxoguanine (oxoG), was shown to induce small deletions, but the mechanism of this phenomenon is currently unknown. We studied the aberrant repair of oxoG located in one- and two-nucleotide bulges by the Escherichia coli and human base excision repair systems. Our results indicate that the repair in such substrates can serve as a mechanism for fixing small deletions in bacteria but not in humans.
DNA 损伤的存在会增加 DNA 复制错误的可能性，并促进突变的发生。特别是，在损伤部位 DNA 聚合酶的暂停会导致聚合酶滑动，并形成 1-2 个核苷酸的凸起。使用未受损的 DNA 模板修复这些结构会导致小的缺失。8-氧鸟嘌呤（oxoG）是最丰富的氧化 DNA 损伤之一，被证明会诱导小的缺失，但目前尚不清楚这种现象的机制。我们研究了大肠杆菌和人类碱基切除修复系统对位于一个和两个核苷酸凸起中的 oxoG 的异常修复。我们的结果表明，这种底物的修复可以作为细菌中小缺失固定的机制，但在人类中则不是。
