ArticleNucleic acids research2011
Replication fork stalling by bulky DNA damage: localization at active origins and checkpoint modulation.
Article in Nucleic acids research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 37 citations in OpenAlex.
- Topological stress regulates replication fork dynamics in unperturbed S phase.Nature communications · 2026Article
- An ATM-PPM1D Circuit Controls the Processing and Restart of DNA Replication Forks.bioRxiv : the preprint server for biology · 2025Article
- The intra-S phase checkpoint directly regulates replication elongation to preserve the integrity of stalled replisomes.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Interindividual Differences in DNA Adduct Formation and Detoxification of 1,3-Butadiene-Derived Epoxide in Human HapMap Cell Lines.Chemical research in toxicology · 2020Article
- TonEBP Regulates PCNA Polyubiquitination in Response to DNA Damage through Interaction with SHPRH and USP1.iScience · 2019Article
- The NuA4 acetyltransferase and histone H4 acetylation promote replication recovery after topoisomerase I-poisoning.Epigenetics & chromatin · 2019Article
- Patterns and mechanisms of structural variations in human cancer.Experimental & molecular medicine · 2018Review
- Mapping DNA damage-dependent genetic interactions in yeast via party mating and barcode fusion genetics.Molecular systems biology · 2018Article
- Transcriptional Profiling ofG3 (Bethesda, Md.) · 2018Article
- Replication fork slowing and stalling are distinct, checkpoint-independent consequences of replicating damaged DNA.PLoS genetics · 2017Article
- Article
- BothAIMS genetics · 2017Article
- Sister chromatid telomere fusions, but not NHEJ-mediated inter-chromosomal telomere fusions, occur independently of DNA ligases 3 and 4.Genome research · 2016Article
- Screening Nonionic Surfactants for Enhanced Biodegradation of Polycyclic Aromatic Hydrocarbons Remaining in Soil After Conventional Biological Treatment.Environmental science & technology · 2016Article
- DNA double-strand break repair is impaired in presenescent Syrian hamster fibroblasts.BMC molecular biology · 2015Article
- DNA damage response in neonatal and adult stromal cells compared with induced pluripotent stem cells.Stem cells translational medicine · 2015Article
- The challenges and importance of structural variation detection in livestock.Frontiers in genetics · 2014Review
- Mitomycin C reduces abundance of replication forks but not rates of fork progression in primary and transformed human cells.Oncoscience · 2014Article
- Replicating damaged DNA in eukaryotes.Cold Spring Harbor perspectives in biology · 2013Review
- Impaired replication elongation in Tetrahymena mutants deficient in histone H3 Lys 27 monomethylation.Genes & development · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The integrity of the genome is threatened by DNA damage that blocks the progression of replication forks. Little is known about the genomic locations of replication fork stalling, and its determinants and consequences in vivo. Here we show that bulky DNA damaging agents induce localized fork stalling at yeast replication origins, and that localized stalling is dependent on proximal origin activity and is modulated by the intra-S-phase checkpoint. Fork stalling preceded the formation of sister chromatid junctions required for bypassing DNA damage. Despite DNA adduct formation, localized fork stalling was abrogated at an origin inactivated by a point mutation and prominent stalling was not detected at naturally-inactive origins in the replicon. The intra-S-phase checkpoint contributed to the high-level of fork stalling at early origins, while checkpoint inactivation led to initiation, localized stalling and chromatid joining at a late origin. Our results indicate that replication forks initially encountering a bulky DNA adduct exhibit a dual nature of stalling: a checkpoint-independent arrest that triggers sister chromatid junction formation, as well as a checkpoint-enhanced arrest at early origins that accompanies the repression of late origin firing. We propose that the initial checkpoint-enhanced arrest reflects events that facilitate fork resolution at subsequent lesions.
Indexed as
Identifiers
What OpenQuestion holds
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.