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DNA Polymerase II Supports the Replicative Bypass of N2-Alkyl-2-deoxyguanosine Lesions in Escherichia coli Cells.

Abstract

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.

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