Alkylation represents a main form of DNA damage. The N² position of guanine is frequently alkylated in DNA. The SOS-induced polymerases have been shown to be capable of bypassing various DNA damage products in Escherichia coli. Herein, we explored the influences of four N²-alkyl-dG lesions (alkyl = ethyl, n-butyl, isobutyl, or sec-butyl) on DNA replication in AB1157 E. coli cells and the corresponding strains with polymerases (Pol) II, IV, and V being individually or simultaneously knocked out. We found that N²-Et-dG is slightly less blocking to DNA replication than the N²-Bu-dG lesions, which display very similar replication bypass efficiencies. Additionally, Pol II and, to a lesser degree, Pol IV and Pol V are required for the efficient bypass of the N²-alkyl-dG adducts, and none of these lesions was mutagenic. Together, our results support that the efficient replication across small N²-alkyl-dG DNA adducts in E. coli depends mainly on Pol II.

中文翻译：

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DNA 聚合酶 II 支持大肠杆菌细胞中 N2-烷基-2'-脱氧鸟苷损伤的复制旁路

烷基化是 DNA 损伤的主要形式。鸟嘌呤的N ²位在 DNA 中经常被烷基化。SOS 诱导的聚合酶已被证明能够绕过大肠杆菌中的各种 DNA 损伤产物。在此，我们探讨了四种N ² -烷基-dG 损伤（烷基 = 乙基、正丁基、异丁基或仲丁基）对 AB1157大肠杆菌细胞和具有聚合酶 (Pol) II 的相应菌株中 DNA 复制的影响、IV 和 V 被单独或同时淘汰。我们发现N ^{2 -Et-dG 对 DNA 复制的阻断比}N ²稍小-Bu-dG 病变，显示非常相似的复制绕过效率。此外， N ² -烷基-dG 加合物的有效旁路需要 Pol II 以及在较小程度上的 Pol IV 和 Pol V ，并且这些损伤都不是诱变的。总之，我们的结果支持大肠杆菌中小N ² -烷基-dG DNA 加合物的有效复制主要取决于 Pol II。