ArticleMolecular and cellular biology2003
Schizosaccharomyces pombe checkpoint response to DNA interstrand cross-links.
Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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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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Who cites it
18 citing papers in PubMed, 33 citations in OpenAlex.
- Dual targeting of Saccharomyces cerevisiae Pso2 to mitochondria and the nucleus, and its functional relevance in the repair of DNA interstrand crosslinks.G3 (Bethesda, Md.) · 2022Article
- The roles of fission yeast exonuclease 5 in nuclear and mitochondrial genome stability.DNA repair · 2019Article
- Identification of S-phase DNA damage-response targets in fission yeast reveals conservation of damage-response networks.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- The extent of error-prone replication restart by homologous recombination is controlled by Exo1 and checkpoint proteins.Journal of cell science · 2014Article
- Pre-activation of the genome integrity checkpoint increases DNA damage tolerance.Nucleic acids research · 2013Article
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- Impediments to replication fork movement: stabilisation, reactivation and genome instability.Chromosoma · 2013Review
- The RecQ4 orthologue Hrq1 is critical for DNA interstrand cross-link repair and genome stability in fission yeast.Molecular and cellular biology · 2012Article
- Radiosensitivity and repair kinetics of gamma-irradiated leukocytes from sporadic prostate cancer patients and healthy individuals assessed by alkaline comet assay.Iranian biomedical journal · 2010Article
- The Schizosaccharomyces pombe checkpoint kinases Chk1 and Cds1 are important for cell survival in response to cisplatin.PloS one · 2009Article
- Checkpoint responses to unusual structures formed by DNA repeats.Molecular carcinogenesis · 2009Review
- Human immunodeficiency virus type 1 Vpr induces cell cycle G2 arrest through Srk1/MK2-mediated phosphorylation of Cdc25.Journal of virology · 2008Article
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- Unwind and slow down: checkpoint activation by helicase and polymerase uncoupling.Genes & development · 2005Article
- A Tel1/MRX-dependent checkpoint inhibits the metaphase-to-anaphase transition after UV irradiation in the absence of Mec1.Molecular and cellular biology · 2004Article
- Fhit-deficient normal and cancer cells are mitomycin C and UVC resistant.British journal of cancer · 2004Article
- Microhomology-dependent end joining and repair of transposon-induced DNA hairpins by host factors in Saccharomyces cerevisiae.Molecular and cellular biology · 2004Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Drugs that produce covalent interstrand cross-links (ICLs) in DNA remain central to the treatment of cancer, but the cell cycle checkpoints activated by ICLs have received little attention. We have used the fission yeast, Schizosaccharomyces pombe, to elucidate the checkpoint responses to the ICL-inducing anticancer drugs nitrogen mustard and mitomycin C. First we confirmed that the repair pathways acting on ICLs in this yeast are similar to those in the main organisms studied to date (Escherichia coli, budding yeast, and mammalian cells), principally nucleotide excision repair and homologous recombination. We also identified and disrupted the S. pombe homologue of the Saccharomyces cerevisiae SNM1/PSO2 ICL repair gene and found that this activity is required for normal resistance to cross-linking agents, but not other forms of DNA damage. Survival and biochemical analysis indicated a key role for the "checkpoint Rad" family acting through the chk1-dependent DNA damage checkpoint in the ICL response. Rhp9-dependent phosphorylation of Chk1 correlates with G(2) arrest following ICL induction. In cells able to bypass the G(2) block, a second-cycle (S-phase) arrest was observed. Only a transient activation of the Cds1 DNA replication checkpoint factor occurs following ICL formation in wild-type cells, but this is increased and persists in G(2) arrest-deficient mutants. This likely reflects the fraction of cells escaping the G(2) damage checkpoint and arresting in the subsequent S phase due to ICL replication blocks. Disruption of cds1 confers increased resistance to ICLs, suggesting that this second-cycle S-phase arrest might be a lethal event.
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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.