ArticlePLoS genetics2015
DNA damage response and spindle assembly checkpoint function throughout the cell cycle to ensure genomic integrity.
Article in PLoS genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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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
43 citing papers in PubMed, 66 citations in OpenAlex.
- Expanding Synthetic Lethality in DNA Damage Response-Defective Cancers Through Stress Phenotype-Guided Kinase Targeting.International journal of molecular sciences · 2026Review
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- PQQ Modulates Cell Cycle and DNA Replication Programs to Alleviate Replicative Senescence in Human Umbilical Cord Mesenchymal Stromal Cells.Stem cell reviews and reports · 2026Article
- Pharmaceutical inhibition of the Chk2 kinase mitigates cone photoreceptor degeneration in an iPSC model of Bardet-Biedl syndrome.iScience · 2025Article
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- Mechanical stress during confined migration causes aberrant mitoses and c-MYC amplification.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Drug repurposing for cancer therapy.Signal transduction and targeted therapy · 2024Review
- The chromatin-associated 53BP1 ortholog, HSR-9, regulates recombinational repair andbioRxiv : the preprint server for biology · 2024Article
- Gross Chromosomal Rearrangement at Centromeres.Biomolecules · 2023Review
- Previous infection with SARS-CoV-2 impacts embryo morphokinetics but not clinical outcomes in a time-lapse imaging system.Molecular reproduction and development · 2023Article
- Identification of activity-induced Egr3-dependent genes reveals genes associated with DNA damage response and schizophrenia.Translational psychiatry · 2022Article
- Deoxyelephantopin Induces Apoptosis and Enhances Chemosensitivity of Colon Cancer via miR-205/Bcl2 Axis.International journal of molecular sciences · 2022Article
- DNA repair, recombination, and damage signaling.Genetics · 2022Review
- Nuclear envelope, chromatin organizers, histones, and DNA: The many achilles heels exploited across cancers.Frontiers in cell and developmental biology · 2022Review
- The Role of the APC/C and Its Coactivators Cdh1 and Cdc20 in Cancer Development and Therapy.Frontiers in genetics · 2022Review
- PIGN spatiotemporally regulates the spindle assembly checkpoint proteins in leukemia transformation and progression.Scientific reports · 2021Article
- Inhibition of Nuclear Pore Complex Formation Selectively Induces Cancer Cell Death.Cancer discovery · 2021Article
- The conserved AAA-ATPase PCH-2Molecular biology of the cell · 2020Article
- Kv10.1 Regulates Microtubule Dynamics during Mitosis.Cancers · 2020Article
- Antagonistic control ofeLife · 2020Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Errors in replication or segregation lead to DNA damage, mutations, and aneuploidies. Consequently, cells monitor these events and delay progression through the cell cycle so repair precedes division. The DNA damage response (DDR), which monitors DNA integrity, and the spindle assembly checkpoint (SAC), which responds to defects in spindle attachment/tension during metaphase of mitosis and meiosis, are critical for preventing genome instability. Here we show that the DDR and SAC function together throughout the cell cycle to ensure genome integrity in C. elegans germ cells. Metaphase defects result in enrichment of SAC and DDR components to chromatin, and both SAC and DDR are required for metaphase delays. During persistent metaphase arrest following establishment of bi-oriented chromosomes, stability of the metaphase plate is compromised in the absence of DDR kinases ATR or CHK1 or SAC components, MAD1/MAD2, suggesting SAC functions in metaphase beyond its interactions with APC activator CDC20. In response to DNA damage, MAD2 and the histone variant CENPA become enriched at the nuclear periphery in a DDR-dependent manner. Further, depletion of either MAD1 or CENPA results in loss of peripherally associated damaged DNA. In contrast to a SAC-insensitive CDC20 mutant, germ cells deficient for SAC or CENPA cannot efficiently repair DNA damage, suggesting that SAC mediates DNA repair through CENPA interactions with the nuclear periphery. We also show that replication perturbations result in relocalization of MAD1/MAD2 in human cells, suggesting that the role of SAC in DNA repair is conserved.
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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.