ReviewBiomolecules2015
Managing Single-Stranded DNA during Replication Stress in Fission Yeast.
Review in Biomolecules, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 33 citations in OpenAlex.
- STN1 upregulation promotes PARPi resistance in BRCA2-deficient cancer cells via replication fork protection and suppression of ssDNA gap formation.NAR cancer · 2026Article
- STN1 upregulation promotes PARPi resistance in BRCA2-deficient cancer cells via replication fork protection and suppression of ssDNA gap formation.bioRxiv : the preprint server for biology · 2026Article
- Replication Stress in Activated Human NK Cells Induces Sensitivity to Apoptosis.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Extracellular Self-DNA Effects on Yeast Cell Cycle and Transcriptome during Batch Growth.Biomolecules · 2024Article
- Rapid Long-distance Migration of RPA on Single Stranded DNA Occurs Through Intersegmental Transfer Utilizing Multivalent Interactions.Journal of molecular biology · 2024Article
- Chromodomain mutation in S. pombe Kat5/Mst1 affects centromere dynamics and DNA repair.PloS one · 2024Article
- Extracellular DNA secreted in yeast cultures is metabolism-specific and inhibits cell proliferation.Microbial cell (Graz, Austria) · 2023Article
- Determinants of RPA megafoci localization to the nuclear periphery in response to replication stress.G3 (Bethesda, Md.) · 2022Article
- Supercoiling and looping promote DNA base accessibility and coordination among distant sites.Nature communications · 2021Article
- MonitoringBiology open · 2021Article
- Checkpoint Regulation of Nuclear Tos4 Defines S Phase Arrest in Fission Yeast.G3 (Bethesda, Md.) · 2020Article
- Mrc1 and Tof1 prevent fragility and instability at long CAG repeats by their fork stabilizing function.Nucleic acids research · 2019Article
- Construction of Designer Selectable Marker Deletions with a CRISPR-Cas9 Toolbox inG3 (Bethesda, Md.) · 2018Article
- Lingering single-strand breaks trigger Rad51-independent homology-directed repair of collapsed replication forks in the polynucleotide kinase/phosphatase mutant of fission yeast.PLoS genetics · 2017Article
- Replication fork slowing and stalling are distinct, checkpoint-independent consequences of replicating damaged DNA.PLoS genetics · 2017Article
- Shelterin components mediate genome reorganization in response to replication stress.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
Replication fork stalling generates a variety of responses, most of which cause an increase in single-stranded DNA. ssDNA is a primary signal of replication distress that activates cellular checkpoints. It is also a potential source of genome instability and a substrate for mutation and recombination. Therefore, managing ssDNA levels is crucial to chromosome integrity. Limited ssDNA accumulation occurs in wild-type cells under stress. In contrast, cells lacking the replication checkpoint cannot arrest forks properly and accumulate large amounts of ssDNA. This likely occurs when the replication fork polymerase and helicase units are uncoupled. Some cells with mutations in the replication helicase (mcm-ts) mimic checkpoint-deficient cells, and accumulate extensive areas of ssDNA to trigger the G2-checkpoint. Another category of helicase mutant (mcm4-degron) causes fork stalling in early S-phase due to immediate loss of helicase function. Intriguingly, cells realize that ssDNA is present, but fail to detect that they accumulate ssDNA, and continue to divide. Thus, the cellular response to replication stalling depends on checkpoint activity and the time that replication stress occurs in S-phase. In this review we describe the signs, signals, and symptoms of replication arrest from an ssDNA perspective. We explore the possible mechanisms for these effects. We also advise the need for caution when detecting and interpreting data related to the accumulation of ssDNA.
Indexed as
Identifiers
What OpenQuestion holds
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.