ArticleScientific reports2016
DNA replication inhibitor hydroxyurea alters Fe-S centers by producing reactive oxygen species in vivo.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 54 citations in OpenAlex.
- Hydroxyurea in the management of sickle cell disease-associated priapism: a scoping review.International journal of impotence research · 2026Article
- Mechanisms of Hydroxyurea-Mediated DNA Damage Potentiation in Fanconi Anemia Cells.International journal of molecular sciences · 2026Article
- Hydroxyurea modulates thiol-disulfide homeostasis in the yeast endoplasmic reticulum.Life science alliance · 2025Article
- Control of Replication Stress Response by Cytosolic Fe-S Cluster Assembly (CIA) Machinery.Cells · 2025Review
- Genome-wide conditional degron libraries for functional genomics.The Journal of cell biology · 2025Article
- Characterizing the regulatory effects of H2A.Z and SWR1-C on gene expression during hydroxyurea exposure in Saccharomyces cerevisiae.PLoS genetics · 2025Article
- Revised mechanism of hydroxyurea-induced cell cycle arrest and an improved alternative.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Embryonic stem cells maintain high origin activity and slow forks to coordinate replication with cell cycle progression.EMBO reports · 2024Article
- Characteristic effect of hydroxyurea on the higher-order structure of DNA and gene expression.Scientific reports · 2024Article
- Effect of Hydroxyurea on Morphology, Proliferation, and Protein Expression onInternational journal of molecular sciences · 2024Article
- Induction of Oxidative Stress in Sirtuin Gene-Disrupted Ashbya gossypii Mutants Overproducing Riboflavin.Molecular biotechnology · 2024Article
- Oxidative replication stress induced by long-term exposure to hydroxyurea in root meristem cells of Vicia faba.Plant cell reports · 2024Article
- Excessive reactive oxygen species induce transcription-dependent replication stress.Nature communications · 2023Article
- The identification of viral ribonucleotide reductase encoded by ORF23 and ORF141 genes and effect on CyHV-2 replication.Frontiers in microbiology · 2023Article
- Metabolic remodeling maintains a reducing environment for rapid activation of the yeast DNA replication checkpoint.The EMBO journal · 2022Article
- Homologous Recombination as a Fundamental Genome Surveillance Mechanism during DNA Replication.Genes · 2021Review
- Biochemical Evaluation of the Effects of Hydroxyurea in Vitro on Red Blood Cells.Antioxidants (Basel, Switzerland) · 2021Article
- The stabilized Pol31-Pol3 interface counteracts Pol32 ablation with differential effects on repair.Life science alliance · 2021Article
- Hydroxyurea-The Good, the Bad and the Ugly.Genes · 2021Review
- Hydroxyurea Induces a Stress Response That Alters DNA Replication and Nucleotide Metabolism in Bacillus subtilis.Journal of bacteriology · 2021Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Redox homeostasis is tightly controlled in cells as it is critical for most cellular functions. Iron-Sulfur centers (Fe-S) are metallic cofactors with electronic properties that are associated with proteins and allow fine redox tuning. Following the observation that altered Fe-S biosynthesis is correlated with a high sensitivity to hydroxyurea (HU), a potent DNA replication blocking agent, we identified that oxidative stress response pathway under the control of the main regulator Yap1 attenuates HU deleterious effects, as it significantly increases resistance to HU, Fe-S biosynthesis and DNA replication kinetics in the presence of HU. Yap1 effect is mediated at least in part through up-regulation of two highly conserved genes controlling cytosolic Fe-S biosynthesis and oxidative stress, Dre2 and Tah18. We next observed that HU produces deleterious effects on cytosolic Fe-S clusters in proteins in vivo but not in vitro, suggesting that HU's impact on Fe-S in vivo is mediated by cellular metabolism. Finally, we evidenced that HU exposure was accompanied by production of reactive oxygen species intracellularly. Altogether, this study provides mechanistic insight on the initial observation that mutants with altered Fe-S biosynthesis are highly sensitive to HU and uncovers a novel mechanism of action of this widely used DNA replication inhibitor.
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