ArticleMolecular and cellular biology2007
The intra-S-phase checkpoint affects both DNA replication initiation and elongation: single-cell and -DNA fiber analyses.
Article in Molecular and cellular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 151 papers.
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Who cites it
151 citing papers in PubMed, 224 citations in OpenAlex.
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- Topoisomerase I inhibition suppresses nuclear blebbing via RNA Pol II stalling and nuclear stiffening.bioRxiv : the preprint server for biology · 2026Article
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- DNA damage-induced phosphorylation of a replicative DNA helicase results in inhibition of DNA replication through attenuation of helicase function.Nucleic acids research · 2024Article
- MRE11 and TREX1 control senescence by coordinating replication stress and interferon signaling.Nature communications · 2024Article
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- Embracing Heterogeneity: Challenging the Paradigm of Replisomes as Deterministic Machines.Chemical reviews · 2023Review
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- Ring finger protein 126 promotes breast cancer metastasis and serves as a potential target to improve the therapeutic sensitivity of ATR inhibitors.Breast cancer research : BCR · 2022Article
- Walking a tightrope: The complex balancing act of R-loops in genome stability.Molecular cell · 2022Review
- Non-enzymatic function of WRN RECQL helicase regulates removal of topoisomerase-I-DNA covalent complexes and triggers NF-κB signaling in cancer.Aging cell · 2022Article
- Chl1 helicase controls replication fork progression by regulating dNTP pools.Life science alliance · 2022Article
- Replication-dependent cytotoxicity and Spartan-mediated repair of trapped PARP1-DNA complexes.Nucleic acids research · 2021Article
- Review
- Rad53 checkpoint kinase regulation of DNA replication fork rate via Mrc1 phosphorylation.eLife · 2021Article
- Organization of DNA Replication Origin Firing inGenes · 2021Article
- SLFN11 Inactivation Induces Proteotoxic Stress and Sensitizes Cancer Cells to Ubiquitin Activating Enzyme Inhibitor TAK-243.Cancer research · 2021Article
91 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
To investigate the contribution of DNA replication initiation and elongation to the intra-S-phase checkpoint, we examined cells treated with the specific topoisomerase I inhibitor camptothecin. Camptothecin is a potent anticancer agent producing well-characterized replication-mediated DNA double-strand breaks through the collision of replication forks with topoisomerase I cleavage complexes. After a short dose of camptothecin in human colon carcinoma HT29 cells, DNA replication was inhibited rapidly and did not recover for several hours following drug removal. That inhibition occurred preferentially in late-S-phase, compared to early-S-phase, cells and was due to both an inhibition of initiation and elongation, as determined by pulse-labeling nucleotide incorporation in replication foci and DNA fibers. DNA replication was actively inhibited by checkpoint activation since 7-hydroxystaurosporine (UCN-01), the specific Chk1 inhibitor CHIR-124, or transfection with small interfering RNA targeting Chk1 restored both initiation and elongation. Abrogation of the checkpoint markedly enhanced camptothecin-induced DNA damage at replication sites where histone gamma-H2AX colocalized with replication foci. Together, our study demonstrates that the intra-S-phase checkpoint is exerted by Chk1 not only upon replication initiation but also upon DNA elongation.
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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.