ArticlePLoS genetics2013
Genome-wide mutation avalanches induced in diploid yeast cells by a base analog or an APOBEC deaminase.
Article in PLoS genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
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Who cites it
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.
- Evolutionary Comparative Analyses of DNA-Editing Enzymes of the Immune System: From 5-Dimensional Description of Protein Structures to Immunological Insights and Applications to Protein Engineering.Frontiers in immunology · 2021Pooled it
- Toward optimizing diversifying base editors for high-throughput mutational scanning studies.Nucleic acids research · 2025Article
- MutaT7ACS synthetic biology · 2024Article
- Exploring the Role of Clustered Mutations in Carcinogenesis and Their Potential Clinical Implications in Cancer.International journal of molecular sciences · 2024Review
- Genetic inhibitors of APOBEC3B-induced mutagenesis.Genome research · 2023Article
- Detection of Primary DNA Lesions by Transient Changes in Mating Behavior in YeastInternational journal of molecular sciences · 2023Article
- Practical Approaches for the YeastInternational journal of molecular sciences · 2023Review
- Polymorphism ofInternational journal of molecular sciences · 2023Article
- FIND-IT: Accelerated trait development for a green evolution.Science advances · 2022Article
- Cytosine base editing systems with minimized off-target effect and molecular size.Nature communications · 2022Article
- Compensation for the absence of the catalytically active half of DNA polymerase ε in yeast by positively selected mutations in CDC28.Genetics · 2021Article
- Polymerase-guided base editing enables in vivo mutagenesis and rapid protein engineering.Nature communications · 2021Article
- Rate volatility and asymmetric segregation diversify mutation burden in cells with mutator alleles.Communications biology · 2021Article
- 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
- Comment on "A commensal strain ofScience advances · 2019Article
- Whole genome sequencing data and analyses of the underlyingData in brief · 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
- Deletion of the DEF1 gene does not confer UV-immutability but frequently leads to self-diploidization in yeast Saccharomyces cerevisiae.DNA repair · 2018Article
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 2 countries.
Funding
Abstract
Genetic information should be accurately transmitted from cell to cell; conversely, the adaptation in evolution and disease is fueled by mutations. In the case of cancer development, multiple genetic changes happen in somatic diploid cells. Most classic studies of the molecular mechanisms of mutagenesis have been performed in haploids. We demonstrate that the parameters of the mutation process are different in diploid cell populations. The genomes of drug-resistant mutants induced in yeast diploids by base analog 6-hydroxylaminopurine (HAP) or AID/APOBEC cytosine deaminase PmCDA1 from lamprey carried a stunning load of thousands of unselected mutations. Haploid mutants contained almost an order of magnitude fewer mutations. To explain this, we propose that the distribution of induced mutation rates in the cell population is uneven. The mutants in diploids with coincidental mutations in the two copies of the reporter gene arise from a fraction of cells that are transiently hypersensitive to the mutagenic action of a given mutagen. The progeny of such cells were never recovered in haploids due to the lethality caused by the inactivation of single-copy essential genes in cells with too many induced mutations. In diploid cells, the progeny of hypersensitive cells survived, but their genomes were saturated by heterozygous mutations. The reason for the hypermutability of cells could be transient faults of the mutation prevention pathways, like sanitization of nucleotide pools for HAP or an elevated expression of the PmCDA1 gene or the temporary inability of the destruction of the deaminase. The hypothesis on spikes of mutability may explain the sudden acquisition of multiple mutational changes during evolution and carcinogenesis.
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Registered trials
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.