ArticleProceedings of the National Academy of Sciences of the United States of America2004
Mutagenesis, genotoxicity, and repair of 1-methyladenine, 3-alkylcytosines, 1-methylguanine, and 3-methylthymine in alkB Escherichia coli.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 146 papers.
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Who cites it
146 citing papers in PubMed, 245 citations in OpenAlex.
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- Assessing the contribution of rare DNA states to cancer mutational signatures using sequence-specific conformational fingerprinting.Research square · 2025Article
- DNA Damage and Repair in Pancreatic Cancer-The Latest Findings.International journal of molecular sciences · 2025Review
- Conformation-Dependent Lesion Bypass and Mutagenicity of Bulky 2-Acetylaminofluorene-Guanine DNA Adduct in Epigenetically Relevant Sequence Contexts.Chemical research in toxicology · 2025Article
- Catalytic Mechanism of the Bacterial Non-Heme Fe(II) and 2-Oxoglutarate Dependent Enzyme AlkB with Single-Stranded DNA Containing Complex Guanine Adducts.Inorganic chemistry · 2025Article
- A human high-fidelity DNA polymerase holoenzyme has a wide range of lesion bypass activities.Nucleic acids research · 2025Article
- Effect of methyl DNA adducts on 3'-5' exonuclease activity of human TREX1.The Biochemical journal · 2025Article
- Nitric oxide inhibits ten-eleven translocation DNA demethylases to regulate 5mC and 5hmC across the genome.Nature communications · 2025Article
- Evaluation of ALKBH2 and ALKBH3 gene regulation in patients with adult T-cell leukemia/lymphoma.Virology journal · 2024Article
- A human high-fidelity DNA polymerase holoenzyme has a wide range of lesion bypass activities.bioRxiv : the preprint server for biology · 2024Article
- Stable Interstrand Cross-Links Generated from the Repair of 1,Journal of the American Chemical Society · 2024Article
- The DNA Alkyltransferase Family of DNA Repair Proteins: Common Mechanisms, Diverse Functions.International journal of molecular sciences · 2023Review
- Conformation-dependent lesion bypass of bulky arylamine-dG adducts generated from 2-nitrofluorene in epigenetic sequence contexts.Nucleic acids research · 2023Article
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86 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
AlkB repairs 1-alkyladenine and 3-methylcytosine lesions in DNA by directly reversing the base damage. Although repair studies with randomly alkylated substrates have been performed, the miscoding nature of these and related individually alkylated bases and the suppression of mutagenesis by AlkB within cells have not yet been explored. Here, we address the miscoding potential of 1-methyldeoxyadenosine (m1A), 3-methyldeoxycytidine (m3C), 3-ethyldeoxycytidine (e3C), 1-methyldeoxyguanosine (m1G), and 3-methyldeoxythymidine (m3T) by synthesizing single-stranded vectors containing each alkylated base, followed by vector passage through Escherichia coli. In SOS(-), AlkB-deficient cells, m1A was only 1% mutagenic; however, m3C and e3C were 30% mutagenic, rising to 70% in SOS(+) cells. In contrast, the mutagenicity of m1G and m3T in AlkB(-) cells dropped slightly when SOS polymerases were expressed (m1G from 80% to 66% and m3T from 60% to 53%). Mutagenicity was abrogated for m1A, m3C, and e3C in wild-type (AlkB(+)) cells, whereas m3T mutagenicity was only partially reduced. Remarkably, m1G mutagenicity was also eliminated in AlkB(+) cells, establishing it as a natural AlkB substrate. All lesions were blocks to replication in AlkB-deficient cells. The m1A, m3C, and e3C blockades were completely removed in wild-type cells; the m1G blockade was partially removed and that for m3T was unaffected by the presence of AlkB. All lesions demonstrated enhanced bypass when SOS polymerases were induced. This work provides direct evidence that AlkB suppresses both genotoxicity and mutagenesis by physiologically realistic low doses of 1-alkylpurine and 3-alkylpyrimidine DNA damage in vivo.
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