ArticleMolecular cell2006
Deregulated replication licensing causes DNA fragmentation consistent with head-to-tail fork collision.
Article in Molecular cell, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 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
89 citing papers in PubMed.
- Replication stress in cancer: origins, consequences and therapeutic opportunities.Nature reviews. Cancer · 2026Review
- CDT1 acts with the replisome to remodel replication forks.Science advances · 2026Article
- FANCD2 restrains fork progression and prevents fragility at early origins upon re-replication.Nature communications · 2026Article
- Overexpression of CDT1 inhibits cell cycle progression at S phase by interacting with the mini-chromosome maintenance complex and causes DNA damage.FEBS open bio · 2026Article
- Characterizing replisome disassembly in human cells.iScience · 2024Article
- RAD51 restricts DNA over-replication from re-activated origins.The EMBO journal · 2024Article
- CDT1 is the major functional regulatory subunit of the pre-replication complex in zygotes.Cell proliferation · 2023Article
- CDT1 inhibits CMG helicase in early S phase to separate origin licensing from DNA synthesis.Molecular cell · 2023Article
- Unscheduled DNA replication in G1 causes genome instability and damage signatures indicative of replication collisions.Nature communications · 2022Article
- Hallmarks of DNA replication stress.Molecular cell · 2022Review
- The Role of MTBP as a Replication Origin Firing Factor.Biology · 2022Review
- Quantitative profiling of adaptation to cyclin E overproduction.Life science alliance · 2022Article
- Cell cycle control in cancer.Nature reviews. Molecular cell biology · 2022Review
- SPOP mutation induces replication over-firing by impairing Geminin ubiquitination and triggers replication catastrophe upon ATR inhibition.Nature communications · 2021Article
- Dynamics of replication origin over-activation.Nature communications · 2021Article
- Aberrant MCM10 SUMOylation induces genomic instability mediated by a genetic variant associated with survival of esophageal squamous cell carcinoma.Clinical and translational medicine · 2021Article
- Article
- A Different View for an Old Disease: NEDDylation and Other Ubiquitin-Like Post-Translational Modifications in Chronic Lymphocytic Leukemia.Frontiers in oncology · 2021Review
- Under-Replicated DNA: The Byproduct of Large Genomes?Cancers · 2020Review
- Review
29 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Correct regulation of the replication licensing system ensures that no DNA is rereplicated in a single cell cycle. When the licensing protein Cdt1 is overexpressed in G2 phase of the cell cycle, replication origins are relicensed and the DNA is rereplicated. At the same time, checkpoint pathways are activated that block further cell cycle progression. We have studied the consequence of deregulating the licensing system by adding recombinant Cdt1 to Xenopus egg extracts. We show that Cdt1 induces checkpoint activation and the appearance of small fragments of double-stranded DNA. DNA fragmentation and strong checkpoint activation are dependent on uncontrolled rereplication and do not occur after a single coordinated round of rereplication. The DNA fragments are composed exclusively of rereplicated DNA. The unusual characteristics of these fragments suggest that they result from head-to-tail collision (rear ending) of replication forks chasing one another along the same DNA template.
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Registered trials
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