ArticleeLife2014
Active RNAP pre-initiation sites are highly mutated by cytidine deaminases in yeast, with AID targeting small RNA genes.
Article in eLife, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 60 citations in OpenAlex.
- Unraveling the lexicon of complex mutational phenomena in human cancers.Nature cancer · 2026Review
- Break-induced replication forms long mutable single-strand DNA during meiosis.Nature communications · 2026Article
- Defining APOBEC-induced mutation signatures and modifying activities in yeast.Methods in enzymology · 2025Article
- Article
- Distinguishing preferences of human APOBEC3A and APOBEC3B for cytosines in hairpin loops, and reflection of these preferences in APOBEC-signature cancer genome mutations.Nature communications · 2024Article
- Glycidamide-induced hypermutation in yeast single-stranded DNA reveals a ubiquitous clock-like mutational motif in humans.Nucleic acids research · 2023Article
- Human activation-induced deaminase lacks strong replicative strand bias or preference for cytosines in hairpin loops.Nucleic acids research · 2022Article
- Single-stranded DNA binding proteins influence APOBEC3A substrate preference.Scientific reports · 2021Article
- Analysis of gene expression and mutation data points on contribution of transcription to the mutagenesis by APOBEC enzymes.NAR cancer · 2021Article
- AID in Chronic Lymphocytic Leukemia: Induction and Action During Disease Progression.Frontiers in oncology · 2021Review
- Analysis of APOBEC-induced mutations in yeast strains with low levels of replicative DNA polymerases.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- The spectrum of APOBEC3 activity: From anti-viral agents to anti-cancer opportunities.DNA repair · 2019Review
- Genome-wide mapping of regions preferentially targeted by the human DNA-cytosine deaminase APOBEC3A using uracil-DNA pulldown and sequencing.The Journal of biological chemistry · 2019Article
- Nucleotide Weight Matrices Reveal Ubiquitous Mutational Footprints of AID/APOBEC Deaminases in Human Cancer Genomes.Cancers · 2019Article
- Guidelines for DNA recombination and repair studies: Cellular assays of DNA repair pathways.Microbial cell (Graz, Austria) · 2019Review
- Mutational signatures and mutable motifs in cancer genomes.Briefings in bioinformatics · 2018Review
- Transfer RNA genes experience exceptionally elevated mutation rates.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Review
- DNA polymerase η mutational signatures are found in a variety of different types of cancer.Cell cycle (Georgetown, Tex.) · 2018Article
- Enzyme cycling contributes to efficient induction of genome mutagenesis by the cytidine deaminase APOBEC3B.Nucleic acids research · 2017Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Cytidine deaminases are single stranded DNA mutators diversifying antibodies and restricting viral infection. Improper access to the genome leads to translocations and mutations in B cells and contributes to the mutation landscape in cancer, such as kataegis. It remains unclear how deaminases access double stranded genomes and whether off-target mutations favor certain loci, although transcription and opportunistic access during DNA repair are thought to play a role. In yeast, AID and the catalytic domain of APOBEC3G preferentially mutate transcriptionally active genes within narrow regions, 110 base pairs in width, fixed at RNA polymerase initiation sites. Unlike APOBEC3G, AID shows enhanced mutational preference for small RNA genes (tRNAs, snoRNAs and snRNAs) suggesting a putative role for RNA in its recruitment. We uncover the high affinity of the deaminases for the single stranded DNA exposed by initiating RNA polymerases (a DNA configuration reproduced at stalled polymerases) without a requirement for specific cofactors.
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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.