ArticleGenes & development2002
ORC and the intra-S-phase checkpoint: a threshold regulates Rad53p activation in S phase.
Article in Genes & development, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 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
120 citing papers in PubMed, 211 citations in OpenAlex.
- Switch from canonical to recombination-dependent DNA synthesis by M-CDK phosphorylation of DNA Polα.The EMBO journal · 2026Article
- The RPA-binding domain and the KKRK motif in Rad26ATRIP cooperate at the perturbed DNA replication fork for initiating checkpoint signalling.PLoS genetics · 2026Article
- A Trade-Off between Body Mass and Cancer Resistance in Cetaceans Is Mediated by Cell Cycle-Related Gene Evolution.Molecular biology and evolution · 2025Article
- DNA Damage and Replication Stress Checkpoints.Annual review of biochemistry · 2025Review
- Dual DNA replication modes: varying fork speeds and initiation rates within the spatial replication program in Xenopus.Nucleic acids research · 2025Article
- EXO1 and DNA2-mediated ssDNA gap expansion is essential for ATR activation and to maintain viability in BRCA1-deficient cells.Nucleic acids research · 2024Article
- RNase H2 degrades toxic RNA:DNA hybrids behind stalled forks to promote replication restart.The EMBO journal · 2023Article
- The increase in cell death rates in caloric restricted cells of the yeast helicase mutant rrm3 is Sir complex dependent.Scientific reports · 2023Article
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- Replisome-cohesin interactions provided by the Tof1-Csm3 and Mrc1 cohesion establishment factors.Chromosoma · 2023Article
- ORChestra coordinates the replication and repair music.BioEssays : news and reviews in molecular, cellular and developmental biology · 2023Article
- The DNA damage checkpoint: A tale from budding yeast.Frontiers in genetics · 2022Review
- Chemical rescue of mutant proteins in living Saccharomyces cerevisiae cells by naturally occurring small molecules.G3 (Bethesda, Md.) · 2021Article
- Who gets a license: DNA synthesis in quiescent cells re-entering the cell cycle.Current genetics · 2021Review
- Chromatin structure restricts origin utilization when quiescent cells re-enter the cell cycle.Nucleic acids research · 2021Article
- Cdc7 activates replication checkpoint by phosphorylating the Chk1-binding domain of Claspin in human cells.eLife · 2019Article
- AMolecular and cellular biology · 2019Article
- The effects of manipulating levels of replication initiation factors on origin firing efficiency in yeast.PLoS genetics · 2019Article
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60 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 at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The intra-S-phase checkpoint in yeast responds to stalled replication forks by activating the ATM-like kinase Mec1 and the CHK2-related kinase Rad53, which in turn inhibit spindle elongation and late origin firing and lead to a stabilization of DNA polymerases at arrested forks. A mutation that destabilizes the second subunit of the Origin Recognition Complex, orc2-1, reduces the number of functional replication forks by 30% and severely compromises the activation of Rad53 by replication stress or DNA damage in S phase. We show that the restoration of the checkpoint response correlates in a dose-dependent manner with the restoration of pre-replication complex formation in G1. Other forms of DNA damage can compensate for the reduced level of fork-dependent signal in the orc2-1 mutant, yet even in wild-type cells, the amount of damage required for Rad53 activation is higher in S phase than in G2. Our data suggest the existence of an S-phase-specific threshold that may be necessary to allow cells to tolerate damage-like DNA structures present at normal replication forks.
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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.