ArticleGenome research2015
Break-seq reveals hydroxyurea-induced chromosome fragility as a result of unscheduled conflict between DNA replication and transcription.
Article in Genome research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
58 citing papers in PubMed, 82 citations in OpenAlex.
- Genome-wide mapping of replication stress response factors reveals the management of polycistronic transcription, replication initiation, and responses to replication stress in Leishmania.Nucleic acids research · 2026Article
- Mechanisms of Hydroxyurea-Mediated DNA Damage Potentiation in Fanconi Anemia Cells.International journal of molecular sciences · 2026Article
- Apoptosis-driven chromosomal rearrangements in cancer: CAD cleavage, nuclear architecture, and microhomology-mediated end joining.Oncogenesis · 2026Review
- From junk to deleterious: Natural subtelomeric repeat amplifications impact fitness and cellular phenotypes in yeast.bioRxiv : the preprint server for biology · 2026Article
- Decoding DNA metabolism and its clinical relevance through the lens of high-throughput sequencing assays.Medical review (2021) · 2026Review
- Induced DNA double strand breaks by genotoxic drugs occur at active transcription H3K36 tri-methylation sites.Communications biology · 2026Article
- The interplay of DNA damage, epigenetics and tumour heterogeneity in driving cancer cell fitness.Nature communications · 2025Review
- Causes and consequences of DNA double-stranded breaks in cardiovascular disease.Molecular and cellular biochemistry · 2025Review
- Precise Mapping of Physiological DSBs Using In-Suspension Break Labeling In Situ and Sequencing (sBLISS).Methods in molecular biology (Clifton, N.J.) · 2025Article
- PHF2-mediated H3K9me balance orchestrates heterochromatin stability and neural progenitor proliferation.EMBO reports · 2024Article
- Characteristic effect of hydroxyurea on the higher-order structure of DNA and gene expression.Scientific reports · 2024Article
- Storage cell proliferation during somatic growth establishes that tardigrades are not eutelic organisms.Biology open · 2024Article
- DNA Damage Atlas: an atlas of DNA damage and repair.Nucleic acids research · 2024Article
- The increase in cell death rates in caloric restricted cells of the yeast helicase mutant rrm3 is Sir complex dependent.Scientific reports · 2023Article
- Hydroxyurea and inactivation of checkpoint kinase MEC1 inhibit transcription termination and pre-mRNA cleavage at polyadenylation sites in budding yeast.Scientific reports · 2023Article
- The MRN complex maintains the biliary-derived hepatocytes in liver regeneration through ATR-Chk1 pathway.NPJ Regenerative medicine · 2023Article
- Excessive reactive oxygen species induce transcription-dependent replication stress.Nature communications · 2023Article
- The yeast Dbf4 ZnCurrent genetics · 2022Article
- Genome-wide mapping of genomic DNA damage: methods and implications.Cellular and molecular life sciences : CMLS · 2021Review
- Hydroxyurea-The Good, the Bad and the Ugly.Genes · 2021Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
We have previously demonstrated that in Saccharomyces cerevisiae replication, checkpoint inactivation via a mec1 mutation leads to chromosome breakage at replication forks initiated from virtually all origins after transient exposure to hydroxyurea (HU), an inhibitor of ribonucleotide reductase. Here we sought to determine whether all replication forks containing single-stranded DNA gaps have equal probability of producing double-strand breaks (DSBs) when cells attempt to recover from HU exposure. We devised a new methodology, Break-seq, that combines our previously described DSB labeling with next generation sequencing to map chromosome breaks with improved sensitivity and resolution. We show that DSBs preferentially occur at genes transcriptionally induced by HU. Notably, different subsets of the HU-induced genes produced DSBs in MEC1 and mec1 cells as replication forks traversed a greater distance in MEC1 cells than in mec1 cells during recovery from HU. Specifically, while MEC1 cells exhibited chromosome breakage at stress-response transcription factors, mec1 cells predominantly suffered chromosome breakage at transporter genes, many of which are the substrates of those transcription factors. We propose that HU-induced chromosome fragility arises at higher frequency near HU-induced genes as a result of destabilized replication forks encountering transcription factor binding and/or the act of transcription. We further propose that replication inhibitors can induce unscheduled encounters between replication and transcription and give rise to distinct patterns of chromosome fragile sites.
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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.