ArticlePLoS genetics2015
Disruption of Transcriptional Coactivator Sub1 Leads to Genome-Wide Re-distribution of Clustered Mutations Induced by APOBEC in Active Yeast Genes.
Article in PLoS genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 54 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
- ERCC2 mutations alter the genomic distribution pattern of somatic mutations and are independently prognostic in bladder cancer.Cell genomics · 2024Article
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- Glycidamide-induced hypermutation in yeast single-stranded DNA reveals a ubiquitous clock-like mutational motif in humans.Nucleic acids research · 2023Article
- Spontaneous deamination of cytosine to uracil is biased to the non-transcribed DNA strand in yeast.DNA repair · 2023Article
- Polymorphism ofInternational journal of molecular sciences · 2023Article
- APOBEC3-mediated mutagenesis in cancer: causes, clinical significance and therapeutic potential.Journal of hematology & oncology · 2023Review
- APOBEC mutagenesis is a common process in normal human small intestine.Nature genetics · 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
- Article
- Analysis of gene expression and mutation data points on contribution of transcription to the mutagenesis by APOBEC enzymes.NAR cancer · 2021Article
- Compensation for the absence of the catalytically active half of DNA polymerase ε in yeast by positively selected mutations in CDC28.Genetics · 2021Article
- Stressed DNA replication generates stressed DNA.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- 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
- 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
- Mitochondrially-targeted APOBEC1 is a potent mtDNA mutator affecting mitochondrial function and organismal fitness in Drosophila.Nature communications · 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
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in genomes of species are frequently distributed non-randomly, resulting in mutation clusters, including recently discovered kataegis in tumors. DNA editing deaminases play the prominent role in the etiology of these mutations. To gain insight into the enigmatic mechanisms of localized hypermutagenesis that lead to cluster formation, we analyzed the mutational single nucleotide variations (SNV) data obtained by whole-genome sequencing of drug-resistant mutants induced in yeast diploids by AID/APOBEC deaminase and base analog 6-HAP. Deaminase from sea lamprey, PmCDA1, induced robust clusters, while 6-HAP induced a few weak ones. We found that PmCDA1, AID, and APOBEC1 deaminases preferentially mutate the beginning of the actively transcribed genes. Inactivation of transcription initiation factor Sub1 strongly reduced deaminase-induced can1 mutation frequency, but, surprisingly, did not decrease the total SNV load in genomes. However, the SNVs in the genomes of the sub1 clones were re-distributed, and the effect of mutation clustering in the regions of transcription initiation was even more pronounced. At the same time, the mutation density in the protein-coding regions was reduced, resulting in the decrease of phenotypically detected mutants. We propose that the induction of clustered mutations by deaminases involves: a) the exposure of ssDNA strands during transcription and loss of protection of ssDNA due to the depletion of ssDNA-binding proteins, such as Sub1, and b) attainment of conditions favorable for APOBEC action in subpopulation of cells, leading to enzymatic deamination within the currently expressed genes. This model is applicable to both the initial and the later stages of oncogenic transformation and explains variations in the distribution of mutations and kataegis events in different tumor cells.
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