ArticleDNA repair2008
Rev1 and Polzeta influence toxicity and mutagenicity of Me-lex, a sequence selective N3-adenine methylating agent.
Article in DNA repair, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Comprehensive whole-genome sequencing reveals origins of mutational signatures associated with aging, mismatch repair deficiency and temozolomide chemotherapy.Nucleic acids research · 2025Article
- Rev1 is a base excision repair enzyme with 5'-deoxyribose phosphate lyase activity.Nucleic acids research · 2016Article
- Eukaryotic DNA polymerase ζ.DNA repair · 2015Review
- Starvation promotes REV1 SUMOylation and p53-dependent sensitization of melanoma and breast cancer cells.Cancer research · 2015Article
- Base excision repair.Cold Spring Harbor perspectives in biology · 2013Review
- Synthesis and characterization of DNA minor groove binding alkylating agents.Chemical research in toxicology · 2013Article
- Balancing repair and tolerance of DNA damage caused by alkylating agents.Nature reviews. Cancer · 2012Review
- Histone H3 lysine 56 acetylation and the response to DNA replication fork damage.Molecular and cellular biology · 2012Article
- 3-Methyl-3-deazaadenine, a stable isostere of N3-methyl-adenine, is efficiently bypassed by replication in vivo and by transcription in vitro.DNA repair · 2011Article
- Effect of n3-methyladenine and an isosteric stable analogue on DNA polymerization.Journal of nucleic acids · 2010Article
- XRCC1 deficiency influences the cytotoxicity and the genomic instability induced by Me-lex, a specific inducer of N3-methyladenine.DNA repair · 2010Article
- Mutagenicity of N3-methyladenine: a multi-translesion polymerase affair.Mutation research · 2010Article
- High frequency of genomic deletions induced by Me-lex, a sequence selective N3-adenine methylating agent, at the Hprt locus in Chinese hamster ovary cells.Mutation research · 2009Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
The relative toxicity and mutagenicity of Me-lex, which selectively generates 3-methyladenine (3-MeA), is dependent on the nature of the DNA repair background. Base excision repair (BER)-defective S. cerevisiae strains mag1 and apn1apn2 were both significantly more sensitive to Me-lex toxicity, but only the latter is significantly more prone to Me-lex-induced mutagenesis. To examine the contribution of translesion synthesis (TLS) DNA polymerases in the bypass of Me-lex-induced lesions, the REV3 and REV1 genes were independently deleted in the parental yeast strain and in different DNA repair-deficient derivatives: the nucleotide excision repair (NER)-deficient rad14, and the BER-deficient mag1 or apn1apn2 strains. The strains contained an integrated ADE2 reporter gene under control of the transcription factor p53. A centromeric yeast expression vector containing the wild-type p53 cDNA was treated in vitro with increasing concentrations of Me-lex and transformed into the different yeast strains. The toxicity of Me-lex-induced lesions was evaluated based on the plasmid transformation efficiency compared to the untreated vector, while Me-lex mutagenicity was assessed using the p53 reporter assay. In the present study, we demonstrate that disruption of Polzeta (through deletion of its catalytic subunit coded by REV3) or Rev1 (by REV1 deletion) increased Me-lex lethality and decreased Me-lex mutagenicity in both the NER-defective (rad14) and BER-defective (mag1; apn1apn2) strains. Therefore, Polzeta and Rev1 contribute to resistance of the lethal effects of Me-lex-induced lesions (3-MeA and derived AP sites) by bypassing lesions and fixing some mutations.
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