Open AccessDNA Polymerase II Supports the Replicative Bypass of N2-Alkyl-2′-deoxyguanosine Lesions in Escherichia coli Cells
Author(s) -
Yinan Wang,
Jun Wu,
Jiabin Wu,
Yinsheng Wang
Publication year - 2021
Publication title -
chemical research in toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.031
H-Index - 156
eISSN - 1520-5010
pISSN - 0893-228X
DOI - 10.1021/acs.chemrestox.0c00478
Subject(s) - dna replication , dna polymerase , escherichia coli , guanine , dna , deoxyguanosine , polymerase , alkylation , microbiology and biotechnology , alkyl , chemistry , dna polymerase ii , dna damage , dna synthesis , dna polymerase i , biology , biochemistry , stereochemistry , polymerase chain reaction , gene , nucleotide , reverse transcriptase , organic chemistry , catalysis
Alkylation represents a main form of DNA damage. The N 2 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 N 2 -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 N 2 -Et-dG is slightly less blocking to DNA replication than the N 2 -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 N 2 -alkyl-dG adducts, and none of these lesions was mutagenic. Together, our results support that the efficient replication across small N 2 -alkyl-dG DNA adducts in E. coli depends mainly on Pol II.