ArticleNature communications2016
Hypersensitivity to DNA damage in antephase as a safeguard for genome stability.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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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.
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Who cites it
20 citing papers in PubMed.
- Article
- E2F activity determines mitosis versus whole-genome duplication in G2-arrested cells.Nature communications · 2025Article
- A concise guide to fluorescent cell cycle reporters for live-cell imaging.Frontiers in cell and developmental biology · 2025Review
- APC/C prevents a noncanonical order of cyclin/CDK activity to maintain CDK4/6 inhibitor-induced arrest.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Mitochondrial HNature communications · 2024Article
- FOXO transcription factors as mediators of stress adaptation.Nature reviews. Molecular cell biology · 2024Review
- APC/C prevents non-canonical order of cyclin/CDK activity to maintain CDK4/6 inhibitor-induced arrest.bioRxiv : the preprint server for biology · 2023Article
- MND1 enables homologous recombination in somatic cells primarily outside the context of replication.Molecular oncology · 2023Article
- Nuclear tension controls mitotic entry by regulating cyclin B1 nuclear translocation.The Journal of cell biology · 2022Article
- Double-strand break toxicity is chromatin context independent.Nucleic acids research · 2022Article
- CDK activity sensors: genetically encoded ratiometric biosensors for live analysis of the cell cycle.Biochemical Society transactions · 2022Article
- Adult Neural Stem Cell Migration Is Impaired in a Mouse Model of Alzheimer's Disease.Molecular neurobiology · 2022Article
- Proteins from the DNA Damage Response: Regulation, Dysfunction, and Anticancer Strategies.Cancers · 2021Review
- Resistance of Hypoxic Cells to Ionizing Radiation Is Mediated in Part via Hypoxia-Induced Quiescence.Cells · 2021Article
- Two Interlinked Bistable Switches Govern Mitotic Control in Mammalian Cells.Current biology : CB · 2018Article
- A limited number of double-strand DNA breaks is sufficient to delay cell cycle progression.Nucleic acids research · 2018Article
- Persistent repair intermediates induce senescence.Nature communications · 2018Article
- Orchestration of DNA Damage Checkpoint Dynamics across the Human Cell Cycle.Cell systems · 2017Article
- How the cell cycle enforces senescence.Aging · 2017Article
- Cdk2 strengthens the intra-S checkpoint and counteracts cell cycle exit induced by DNA damage.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation of the DNA-damage response can lead to the induction of an arrest at various stages in the cell cycle. These arrests are reversible in nature, unless the damage is too excessive. Here we find that checkpoint reversibility is lost in cells that are in very late G2, but not yet fully committed to enter mitosis (antephase). We show that antephase cells exit the cell cycle and enter senescence at levels of DNA damage that induce a reversible arrest in early G2. We show that checkpoint reversibility critically depends on the presence of the APC/C inhibitor Emi1, which is degraded just before mitosis. Importantly, ablation of the cell cycle withdrawal mechanism in antephase promotes cell division in the presence of broken chromosomes. Thus, our data uncover a novel, but irreversible, DNA-damage response in antephase that is required to prevent the propagation of DNA damage during cell division.
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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 Socratic graph.