ArticleNature communications2022
Unscheduled DNA replication in G1 causes genome instability and damage signatures indicative of replication collisions.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- CDC7 and APC/CNature communications · 2026Article
- Dynamic regulation of origin firing factors links CDK activity to dormant origin activation.Nature communications · 2026Article
- Dbf4-dependent kinase finetunes Ino80 function at chromosome replication origins.Nature communications · 2026Article
- Apigenin Alleviates Zearalenone-Induced Oxidative Stress and Apoptosis in Swine Testis Cells Through the Wnt Signaling Pathway.Antioxidants (Basel, Switzerland) · 2025Article
- Dynamic regulation of origin firing factors links CDK activity to dormant origin activation.bioRxiv : the preprint server for biology · 2025Article
- LINC01235 Promotes Clonal Evolution through DNA Replication Licensing-Induced Chromosomal Instability in Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Polyploidy mitigates the impact of DNA damage while simultaneously bearing its burden.Cell death discovery · 2024Article
- DNA replication recruits a friend to overcome a challenging break-up.The EMBO journal · 2024Article
- A common mechanism for recruiting the Rrm3 and RTEL1 accessory helicases to the eukaryotic replisome.The EMBO journal · 2024Article
- Dbf4-dependent kinase promotes cell cycle controlled resection of DNA double-strand breaks and repair by homologous recombination.Nature communications · 2024Article
- RAD51 restricts DNA over-replication from re-activated origins.The EMBO journal · 2024Article
- Large tandem duplications in cancer result from transcription and DNA replication collisions.medRxiv : the preprint server for health sciences · 2024Article
- Transcription-Replication Conflicts as a Source of Genome Instability.Annual review of genetics · 2023Review
- A R-loop sensing pathway mediates the relocation of transcribed genes to nuclear pore complexes.Nature communications · 2023Article
- Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA replicates once per cell cycle. Interfering with the regulation of DNA replication initiation generates genome instability through over-replication and has been linked to early stages of cancer development. Here, we engineer genetic systems in budding yeast to induce unscheduled replication in a G1-like cell cycle state. Unscheduled G1 replication initiates at canonical S-phase origins. We quantifiy the composition of replisomes in G1- and S-phase and identified firing factors, polymerase α, and histone supply as factors that limit replication outside S-phase. G1 replication per se does not trigger cellular checkpoints. Subsequent replication during S-phase, however, results in over-replication and leads to chromosome breaks and chromosome-wide, strand-biased occurrence of RPA-bound single-stranded DNA, indicating head-to-tail replication collisions as a key mechanism generating genome instability upon G1 replication. Low-level, sporadic induction of G1 replication induces an identical response, indicating findings from synthetic systems are applicable to naturally occurring scenarios of unscheduled replication initiation.
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