ArticleThe Journal of biological chemistry2015
Genetic Control of Replication through N1-methyladenine in Human Cells.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 30 citations in OpenAlex.
- Assessing the contribution of rare DNA states to cancer mutational signatures using sequence-specific conformational fingerprinting.Nature communications · 2026Article
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- Assessing the contribution of rare DNA states to cancer mutational signatures using sequence-specific conformational fingerprinting.Research square · 2025Article
- WRN and WRNIP1 ATPases impose high fidelity on translesion synthesis by Y-family DNA polymerases.eLife · 2025Article
- Sequence based model using deep neural network and hybrid features for identification of 5-hydroxymethylcytosine modification.Scientific reports · 2024Article
- WRN exonuclease imparts high fidelity on translesion synthesis by Y family DNA polymerases.Genes & development · 2024Article
- DNA Alkylation Damage by Nitrosamines and Relevant DNA Repair Pathways.International journal of molecular sciences · 2023Review
- Multifaceted Nature of DNA Polymerase θ.International journal of molecular sciences · 2023Review
- TEB/POLQ plays dual roles in protecting Arabidopsis from NO-induced DNA damage.Nucleic acids research · 2022Article
- Accurate prediction of RNA 5-hydroxymethylcytosine modification by utilizing novel position-specific gapped k-mer descriptors.Computational and structural biotechnology journal · 2020Article
- iRNA5hmC: The First Predictor to Identify RNA 5-Hydroxymethylcytosine Modifications Using Machine Learning.Frontiers in bioengineering and biotechnology · 2020Article
- Translesion synthesis DNA polymerases η, ι, and ν promote mutagenic replication through the anticancer nucleoside cytarabine.The Journal of biological chemistry · 2019Article
- DNA polymerase θ accomplishes translesion synthesis opposite 1,NGenes & development · 2019Article
- Genetic control of predominantly error-free replication through an acrolein-derived minor-groove DNA adduct.The Journal of biological chemistry · 2018Article
- Translesion synthesis DNA polymerases promote error-free replication through the minor-groove DNA adduct 3-deaza-3-methyladenine.The Journal of biological chemistry · 2017Article
- Mechanism of error-free DNA synthesis across N1-methyl-deoxyadenosine by human DNA polymerase-ι.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
N1-methyl adenine (1-MeA) is formed in DNA by reaction with alkylating agents and naturally occurring methyl halides. The 1-MeA lesion impairs Watson-Crick base pairing and blocks normal DNA replication. Here we identify the translesion synthesis (TLS) DNA polymerases (Pols) required for replicating through 1-MeA in human cells and show that TLS through this lesion is mediated via three different pathways in which Pols ι and θ function in one pathway and Pols η and ζ, respectively, function in the other two pathways. Our biochemical studies indicate that in the Polι/Polθ pathway, Polι would carry out nucleotide insertion opposite 1-MeA from which Polθ would extend synthesis. In the Polη pathway, this Pol alone would function at both the nucleotide insertion and extension steps of TLS, and in the third pathway, Polζ would extend from the nucleotide inserted opposite 1-MeA by an as yet unidentified Pol. Whereas by pushing 1-MeA into the syn conformation and by forming Hoogsteen base pair with the T residue, Polι would carry out TLS opposite 1-MeA, the ability of Polη to replicate through 1-MeA suggests that despite its need for Watson-Crick hydrogen bonding, Polη can stabilize the adduct in its active site. Remarkably, even though Pols η and ι are quite error-prone at inserting nucleotides opposite 1-MeA, TLS opposite this lesion in human cells occurs in a highly error-free fashion. This suggests that the in vivo fidelity of TLS Pols is regulated by factors such as post-translational modifications, protein-protein interactions, and possibly others.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.