ArticleNucleic acids research2014
Transcriptional bypass of regioisomeric ethylated thymidine lesions by T7 RNA polymerase and human RNA polymerase II.
Article in Nucleic acids research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- RNA polymerase tracking along damaged DNA: Impact on DNA repair and mutagenesis.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- DNA lesion bypass and the stochastic dynamics of transcription-coupled repair.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Transcriptional Perturbations of 2,6-Diaminopurine and 2-Aminopurine.ACS chemical biology · 2022Article
- RNA polymerase pausing, stalling and bypass during transcription of damaged DNA: from molecular basis to functional consequences.Nucleic acids research · 2022Review
- Polymerases and DNA Repair in Neurons: Implications in Neuronal Survival and Neurodegenerative Diseases.Frontiers in cellular neuroscience · 2022Review
- Mitochondrial Transcription Factor A Binds to and Promotes Mutagenic Transcriptional Bypass ofAnalytical chemistry · 2021Article
- Transcriptional Bypass of DNA-Protein and DNA-Peptide Conjugates by T7 RNA Polymerase.ACS chemical biology · 2019Article
- 5-Formylcytosine-induced DNA-peptide cross-links reduce transcription efficiency, but do not cause transcription errors in human cells.The Journal of biological chemistry · 2019Article
- Chemical Analysis of DNA Damage.Analytical chemistry · 2018Review
- Mechanism of DNA alkylation-induced transcriptional stalling, lesion bypass, and mutagenesis.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- The Nonbulky DNA Lesions Spiroiminodihydantoin and 5-Guanidinohydantoin Significantly Block Human RNA Polymerase II Elongation in Vitro.Biochemistry · 2017Article
- Translesion synthesis of O4-alkylthymidine lesions in human cells.Nucleic acids research · 2016Article
- Roles of Aag, Alkbh2, and Alkbh3 in the Repair of Carboxymethylated and Ethylated Thymidine Lesions.ACS chemical biology · 2016Article
- Mass Spectrometry-Based Quantitative Strategies for Assessing the Biological Consequences and Repair of DNA Adducts.Accounts of chemical research · 2016Review
- Quantitative measurement of transcriptional inhibition and mutagenesis induced by site-specifically incorporated DNA lesions in vitro and in vivo.Nature protocols · 2015Article
- RNA polymerase II transcriptional fidelity control and its functional interplay with DNA modifications.Critical reviews in biochemistry and molecular biology · 2015Review
- Transcriptional inhibition and mutagenesis induced by N-nitroso compound-derived carboxymethylated thymidine adducts in DNA.Nucleic acids research · 2015Article
Corrections and comments
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4 authors.
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Abstract
Alkylative damage to DNA can be induced by environmental chemicals, endogenous metabolites and some commonly prescribed chemotherapeutic agents. The regioisomeric N3-, O(2)- and O(4)-ethylthymidine (N3-, O(2)- and O(4)-EtdT, respectively) represent an important class of ethylated DNA lesions. Using nonreplicative double-stranded vectors containing an N3-EtdT, O(2)-EtdT or O(4)-EtdT at a defined site in the template strand, herein we examined the effects of these lesions on DNA transcription mediated by single-subunit T7 RNA polymerase or multisubunit human RNA polymerase II in vitro and in human cells. We found that O(4)-EtdT is highly mutagenic and exclusively induces the misincorporation of guanine opposite the lesion, whereas N3-EtdT and O(2)-EtdT display promiscuous miscoding properties during transcription. In addition, N3-EtdT and O(2)-EtdT were found to inhibit strongly DNA transcription in vitro and in certain human cells. Moreover, N3-EtdT, but not O(2)-EtdT or O(4)-EtdT, is an efficient substrate for transcription-coupled nucleotide excision repair. These findings provide new important insights into how these alkylated DNA lesions compromise the flow of genetic information, which may help to understand the risk of these lesions in living cells.
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