ArticleNature communications2020
Ethanol exposure increases mutation rate through error-prone polymerases.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 64 citations in OpenAlex.
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- Heat Shock Factor 1 forms nuclear condensates and restructures the yeast genome before activating target genes.bioRxiv : the preprint server for biology · 2024Article
- Selection for robust metabolism in domesticated yeasts is driven by adaptation to Hsp90 stress.Science (New York, N.Y.) · 2024Article
- Optimal trade-off between boosted tolerance and growth fitness during adaptive evolution of yeast to ethanol shocks.Biotechnology for biofuels and bioproducts · 2024Article
- Biological Basis of Breast Cancer-Related Disparities in Precision Oncology Era.International journal of molecular sciences · 2024Review
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- Drying as an effective method to store soil samples for DNA-based microbial community analyses: a comparative study.Scientific reports · 2024Article
- Multiple DNA repair pathways prevent acetaldehyde-induced mutagenesis in yeast.bioRxiv : the preprint server for biology · 2024Article
- Ethanol induces replication fork stalling and membrane stress in immortalized laryngeal cells.iScience · 2023Article
- Genome instability footprint under rapamycin and hydroxyurea treatments.PLoS genetics · 2023Article
Corrections and comments
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Authors and funding
18 authors at 5 institutions in 5 countries.
Funding
Abstract
Ethanol is a ubiquitous environmental stressor that is toxic to all lifeforms. Here, we use the model eukaryote Saccharomyces cerevisiae to show that exposure to sublethal ethanol concentrations causes DNA replication stress and an increased mutation rate. Specifically, we find that ethanol slows down replication and affects localization of Mrc1, a conserved protein that helps stabilize the replisome. In addition, ethanol exposure also results in the recruitment of error-prone DNA polymerases to the replication fork. Interestingly, preventing this recruitment through mutagenesis of the PCNA/Pol30 polymerase clamp or deleting specific error-prone polymerases abolishes the mutagenic effect of ethanol. Taken together, this suggests that the mutagenic effect depends on a complex mechanism, where dysfunctional replication forks lead to recruitment of error-prone polymerases. Apart from providing a general mechanistic framework for the mutagenic effect of ethanol, our findings may also provide a route to better understand and prevent ethanol-associated carcinogenesis in higher eukaryotes.
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Registered trials
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