ArticleThe Journal of cell biology1998
Entry into mitosis in vertebrate somatic cells is guarded by a chromosome damage checkpoint that reverses the cell cycle when triggered during early but not late prophase.
Article in The Journal of cell biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 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
55 citing papers in PubMed, 132 citations in OpenAlex.
- Fidelity-Ensuring Consistency of Mitosis is Safeguarded by the 53BP1-USP28-p53 Pathway.bioRxiv : the preprint server for biology · 2026Article
- Mitotic errors as triggers of cell death and inflammation.Nature cell biology · 2026Review
- DNA damage in mitosis: SOD1 delays anaphase onset.The FEBS journal · 2025Article
- Distinct characteristics of the DNA damage response in mammalian oocytes.Experimental & molecular medicine · 2024Review
- Oocytes can repair DNA damage during meiosis via a microtubule-dependent recruitment of CIP2A-MDC1-TOPBP1 complex from spindle pole to chromosomes.Nucleic acids research · 2023Article
- Article
- ADAD2 regulates heterochromatin in meiotic and post-meiotic male germ cells via translation of MDC1.Journal of cell science · 2022Article
- The Apparent Requirement for Protein Synthesis during G2 Phase Is due to Checkpoint Activation.Cell reports · 2020Article
- DNA double-strand break repair-pathway choice in somatic mammalian cells.Nature reviews. Molecular cell biology · 2019Review
- Mitotic functions of poly(ADP-ribose) polymerases.Biochemical pharmacology · 2019Review
- MDC1 Interacts with TOPBP1 to Maintain Chromosomal Stability during Mitosis.Molecular cell · 2019Article
- Two-step interphase microtubule disassembly aids spindle morphogenesis.BMC biology · 2018Article
- The control of DNA repair by the cell cycle.Nature cell biology · 2016Review
- TALEN-based generation of a cynomolgus monkey disease model for human microcephaly.Cell research · 2016Article
- Hypersensitivity to DNA damage in antephase as a safeguard for genome stability.Nature communications · 2016Article
- Article
- Femtosecond near-infrared laser microirradiation reveals a crucial role for PARP signaling on factor assemblies at DNA damage sites.Nucleic acids research · 2016Article
- Maintaining Genome Stability in Defiance of Mitotic DNA Damage.Frontiers in genetics · 2016Review
- Double-strand break repair-adox: Restoration of suppressed double-strand break repair during mitosis induces genomic instability.Cancer science · 2014Review
- Mitosis, double strand break repair, and telomeres: a view from the end: how telomeres and the DNA damage response cooperate during mitosis to maintain genome stability.BioEssays : news and reviews in molecular, cellular and developmental biology · 2014Article
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 1 country.
Funding
Abstract
When vertebrate somatic cells are selectively irradiated in the nucleus during late prophase (<30 min before nuclear envelope breakdown) they progress normally through mitosis even if they contain broken chromosomes. However, if early prophase nuclei are similarly irradiated, chromosome condensation is reversed and the cells return to interphase. Thus, the G2 checkpoint that prevents entry into mitosis in response to nuclear damage ceases to function in late prophase. If one nucleus in a cell containing two early prophase nuclei is selectively irradiated, both return to interphase, and prophase cells that have been induced to returned to interphase retain a normal cytoplasmic microtubule complex. Thus, damage to an early prophase nucleus is converted into a signal that not only reverses the nuclear events of prophase, but this signal also enters the cytoplasm where it inhibits e.g., centrosome maturation and the formation of asters. Immunofluorescent analyses reveal that the irradiation-induced reversion of prophase is correlated with the dephosphorylation of histone H1, histone H3, and the MPM2 epitopes. Together, these data reveal that a checkpoint control exists in early but not late prophase in vertebrate cells that, when triggered, reverses the cell cycle by apparently downregulating existing cyclin-dependent kinase (CDK1) activity.
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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.