ArticleMolecular and cellular biology2004
Saccharomyces cerevisiae Rrm3p DNA helicase promotes genome integrity by preventing replication fork stalling: viability of rrm3 cells requires the intra-S-phase checkpoint and fork restart activities.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 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
80 citing papers in PubMed, 122 citations in OpenAlex.
- Nucleosomes represent a crucial target for the intra-S phase checkpoint in response to replication stress.Science advances · 2025Article
- The increase in cell death rates in caloric restricted cells of the yeast helicase mutant rrm3 is Sir complex dependent.Scientific reports · 2023Article
- 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
- Review
- Article
- A Genome-Wide Screen for Genes Affecting Spontaneous Direct-Repeat Recombination inG3 (Bethesda, Md.) · 2020Article
- Saccharomyces cerevisiae Mus81-Mms4 prevents accelerated senescence in telomerase-deficient cells.PLoS genetics · 2020Article
- Review
- Review
- Replication fork stalling elicits chromatin compaction for the stability of stalling replication forks.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Single-molecule live cell imaging of Rep reveals the dynamic interplay between an accessory replicative helicase and the replisome.Nucleic acids research · 2019Article
- Review
- Article
- SUMO E3 ligase Mms21 prevents spontaneous DNA damage induced genome rearrangements.PLoS genetics · 2018Article
- Article
- PP2A Controls Genome Integrity by Integrating Nutrient-Sensing and Metabolic Pathways with the DNA Damage Response.Molecular cell · 2017Article
- A new role for Rrm3 in repair of replication-born DNA breakage by sister chromatid recombination.PLoS genetics · 2017Article
- PIF1 family DNA helicases suppress R-loop mediated genome instability at tRNA genes.Nature communications · 2017Article
- A Novel Rrm3 Function in Restricting DNA Replication via an Orc5-Binding Domain Is Genetically Separable from Rrm3 Function as an ATPase/Helicase in Facilitating Fork Progression.PLoS genetics · 2016Article
- Article
20 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
Abstract
Rrm3p is a 5'-to-3' DNA helicase that helps replication forks traverse protein-DNA complexes. Its absence leads to increased fork stalling and breakage at over 1,000 specific sites located throughout the Saccharomyces cerevisiae genome. To understand the mechanisms that respond to and repair rrm3-dependent lesions, we carried out a candidate gene deletion analysis to identify genes whose mutation conferred slow growth or lethality on rrm3 cells. Based on synthetic phenotypes, the intra-S-phase checkpoint, the SRS2 inhibitor of recombination, the SGS1/TOP3 replication fork restart pathway, and the MRE11/RAD50/XRS2 (MRX) complex were critical for viability of rrm3 cells. DNA damage checkpoint and homologous recombination genes were important for normal growth of rrm3 cells. However, the MUS81/MMS4 replication fork restart pathway did not affect growth of rrm3 cells. These data suggest a model in which the stalled and broken forks generated in rrm3 cells activate a checkpoint response that provides time for fork repair and restart. Stalled forks are converted by a Rad51p-mediated process to intermediates that are resolved by Sgs1p/Top3p. The rrm3 system provides a unique opportunity to learn the fate of forks whose progress is impaired by natural impediments rather than by exogenous DNA damage.
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.