ArticleDNA repair2011
3-Methyl-3-deazaadenine, a stable isostere of N3-methyl-adenine, is efficiently bypassed by replication in vivo and by transcription in vitro.
Article in DNA repair, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed.
- Mechanism of RNA polymerase II stalling by DNA alkylation.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- RNA polymerase II transcriptional fidelity control and its functional interplay with DNA modifications.Critical reviews in biochemistry and molecular biology · 2015Review
- Molecular basis of transcriptional fidelity and DNA lesion-induced transcriptional mutagenesis.DNA repair · 2014Review
- Synthesis and characterization of DNA minor groove binding alkylating agents.Chemical research in toxicology · 2013Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
The goal of the present work was to determine the impact of N3-methyladenine (3-mA), an important lesion generated by many environmental agents and anticancer drugs, on in vivo DNA replication and in vitro RNA transcription. Due to 3-mA chemical instability, the stable isostere 3-methyl-3-deazaadenine (3-m-c(3)A) was site specifically positioned into an oligodeoxynucleotide. The oligomer was, then incorporated into a vector system that is rapidly converted to ssDNA inside yeast cells and requires DNA replication opposite the lesion for plasmid clonal selection. For control purposes, an adenine or a stable apurinic/apyrimidinic (AP)-lesion was placed at the same site. The presence of each lesion in the oligonucleotide was confirmed by MALDI-TOF analysis. Plasmids were then transfected into yeast cells. While the AP-site dramatically reduced plasmid replication in all strains, the 3-m-c(3)A had a slight effect in the rad30 background which significantly increased only in a rev3rad30 background. Considering TLS events opposite 3-m-c(3)A, the lack of Polη was associated with a substantial increase in AT>GC transitions (p=0.0011), while in the absence of Polζ only events derived from an error free bypass were detected. The 3-m-c(3)A also did not affect in vitro transcription, while the AP-site was a strong block to T7 RNA progression when located in the transcribed strand. We conclude that, in these experimental systems, 3-m-c(3)A is efficiently bypassed by replication in vivo and by transcription in vitro.
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Registered trials
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