ArticlePLoS genetics2013
Coordinated degradation of replisome components ensures genome stability upon replication stress in the absence of the replication fork protection complex.
Article in PLoS genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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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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.
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Who cites it
27 citing papers in PubMed, 34 citations in OpenAlex.
- Evolutionarily Conserved but Mechanistically Distinct Mitochondrial Responses to Loss of Timeless/Swi1.Biomolecules · 2026Article
- A systematic overexpression screen identifies cytotoxic genes encoded by the Cluster L1 mycobacteriophage LeBron.G3 (Bethesda, Md.) · 2026Article
- Multiple Regulatory Mechanisms of Post-Translational Modifications and Therapeutic Potential of Mitotic Catastrophe.International journal of molecular sciences · 2026Review
- A systematic quantitative approach comprehensively defines domain-specific functional pathways linked to Schizosaccharomyces pombe heterochromatin regulation.Nucleic acids research · 2024Article
- A systematic quantitative approach comprehensively defines domain-specific functional pathways linked tobioRxiv : the preprint server for biology · 2024Article
- Implications of ubiquitination and the maintenance of replication fork stability in cancer therapy.Bioscience reports · 2023Review
- The TIMELESS effort for timely DNA replication and protection.Cellular and molecular life sciences : CMLS · 2023Review
- Fanconi anemia: current insights regarding epidemiology, cancer, and DNA repair.Human genetics · 2022Review
- Tachykinin-related peptides modulate immune-gene expression in the mealworm beetle Tenebrio molitor L.Scientific reports · 2022Article
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- The NuA4 acetyltransferase and histone H4 acetylation promote replication recovery after topoisomerase I-poisoning.Epigenetics & chromatin · 2019Article
- Inheritance of CENP-A Nucleosomes during DNA Replication Requires HJURP.Developmental cell · 2018Article
- Fission Yeast Sirtuin Hst4 Functions in Preserving Genomic Integrity by Regulating Replisome Component Mcl1.Scientific reports · 2018Article
- New insights into donor directionality of mating-type switching in Schizosaccharomyces pombe.PLoS genetics · 2018Article
- Dependency of Heterochromatin Domains on Replication Factors.G3 (Bethesda, Md.) · 2018Article
- Regulation of Mammalian DNA Replication via the Ubiquitin-Proteasome System.Advances in experimental medicine and biology · 2017Review
- Role of the Polymerase ϵ sub-unit DPB2 in DNA replication, cell cycle regulation and DNA damage response in Arabidopsis.Nucleic acids research · 2016Article
- Swi1Timeless Prevents Repeat Instability at Fission Yeast Telomeres.PLoS genetics · 2016Article
- Functions of Ubiquitin and SUMO in DNA Replication and Replication Stress.Frontiers in genetics · 2016Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
The stabilization of the replisome complex is essential in order to achieve highly processive DNA replication and preserve genomic integrity. Conversely, it would also be advantageous for the cell to abrogate replisome functions to prevent inappropriate replication when fork progression is adversely perturbed. However, such mechanisms remain elusive. Here we report that replicative DNA polymerases and helicases, the major components of the replisome, are degraded in concert in the absence of Swi1, a subunit of the replication fork protection complex. In sharp contrast, ORC and PCNA, which are also required for DNA replication, were stably maintained. We demonstrate that this degradation of DNA polymerases and helicases is dependent on the ubiquitin-proteasome system, in which the SCF(Pof3) ubiquitin ligase is involved. Consistently, we show that Pof3 interacts with DNA polymerase ε. Remarkably, forced accumulation of replisome components leads to abnormal DNA replication and mitotic catastrophes in the absence of Swi1. Swi1 is known to prevent fork collapse at natural replication block sites throughout the genome. Therefore, our results suggest that the cell elicits a program to degrade replisomes upon replication stress in the absence of Swi1. We also suggest that this program prevents inappropriate duplication of the genome, which in turn contributes to the preservation of genomic integrity.
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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.