ArticlePLoS genetics2017
Replication fork slowing and stalling are distinct, checkpoint-independent consequences of replicating damaged DNA.
Article in PLoS genetics, 2017. 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.
- Identification of Fibrillarin and Cajal Bodies Under DNA Replication Stress Conditions in Root Meristem Cells ofInternational journal of molecular sciences · 2025Article
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- Single-molecule analysis of PARP1-G-quadruplex interaction.bioRxiv : the preprint server for biology · 2025Article
- Effects of PCNA Stability on the Formation of Mutations.International journal of molecular sciences · 2024Article
- Transient ZnProceedings of the National Academy of Sciences of the United States of America · 2024Article
- ATR inhibition augments the efficacy of lurbinectedin in small-cell lung cancer.EMBO molecular medicine · 2023Article
- Single-molecule imaging of genome maintenance proteins encountering specific DNA sequences and structures.DNA repair · 2023Review
- Short-term molecular consequences of chromosome mis-segregation for genome stability.Nature communications · 2023Article
- Structures of Mec1/ATR kinase endogenously stimulated by different genotoxins.Cell discovery · 2022Article
- Review
- Replication stress induced by the ribonucleotide reductase inhibitor guanazole, triapine and gemcitabine in fission yeast.FEMS yeast research · 2022Article
- The role of Vitamin E in hip implant-related corrosion and toxicity: Initial outcome.Journal of the mechanical behavior of biomedical materials · 2021Article
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- Who gets a license: DNA synthesis in quiescent cells re-entering the cell cycle.Current genetics · 2021Review
- Hydroxyurea-The Good, the Bad and the Ugly.Genes · 2021Review
- Expression of the cancer-associated DNA polymerase ε P286R in fission yeast leads to translesion synthesis polymerase dependent hypermutation and defective DNA replication.PLoS genetics · 2021Article
- The DNA damage inducible lncRNA SCAT7 regulates genomic integrity and topoisomerase 1 turnover in lung adenocarcinoma.NAR cancer · 2021Article
- CARM1 regulates replication fork speed and stress response by stimulating PARP1.Molecular cell · 2021Article
- High-Throughput Magnetic Actuation Platform for Evaluating the Effect of Mechanical Force on 3D Tumor Microenvironment.Advanced functional materials · 2021Article
Corrections and comments
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Authors and funding
2 authors.
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Abstract
In response to DNA damage during S phase, cells slow DNA replication. This slowing is orchestrated by the intra-S checkpoint and involves inhibition of origin firing and reduction of replication fork speed. Slowing of replication allows for tolerance of DNA damage and suppresses genomic instability. Although the mechanisms of origin inhibition by the intra-S checkpoint are understood, major questions remain about how the checkpoint regulates replication forks: Does the checkpoint regulate the rate of fork progression? Does the checkpoint affect all forks, or only those encountering damage? Does the checkpoint facilitate the replication of polymerase-blocking lesions? To address these questions, we have analyzed the checkpoint in the fission yeast Schizosaccharomyces pombe using a single-molecule DNA combing assay, which allows us to unambiguously separate the contribution of origin and fork regulation towards replication slowing, and allows us to investigate the behavior of individual forks. Moreover, we have interrogated the role of forks interacting with individual sites of damage by using three damaging agents-MMS, 4NQO and bleomycin-that cause similar levels of replication slowing with very different frequency of DNA lesions. We find that the checkpoint slows replication by inhibiting origin firing, but not by decreasing fork rates. However, the checkpoint appears to facilitate replication of damaged templates, allowing forks to more quickly pass lesions. Finally, using a novel analytic approach, we rigorously identify fork stalling events in our combing data and show that they play a previously unappreciated role in shaping replication kinetics in response to DNA damage.
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