Evidence map›Paper›PMID 21930788›Full record

ArticleMolecular and cellular biology2011

ATP-dependent chromatin remodeling factors tune S phase checkpoint activity.

Tracey J Au, Jairo Rodriguez, Jack A Vincent, Toshio Tsukiyama

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.7field-weighted citation impact, top 16% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. The INO80 remodeller in transcription, replication and repair.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017
    Review
  7. Genome maintenance functions of the INO80 chromatin remodeller.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Cloning, purification, crystallization and preliminary X-ray studies of HMO2 from Saccharomyces cerevisiae.Acta crystallographica. Section F, Structural biology communications · 2014
    Article
  14. Review
  15. Article
  16. Article
  17. Chromatin and the genome integrity network.Nature reviews. Genetics · 2013
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Tracey J AuBasic Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA.
Jairo Rodriguez
Jack A Vincent
Toshio Tsukiyama
Fred Hutch Cancer Center · USUniversity of Washington · US

Funding

Molecular analysis of yeast lsw1 and lsw2 complexesR01GM058465 · NIGMS · FRED HUTCHINSON CANCER RESEARCH CENTER · PI TSUKIYAMA, TOSHIO · 1999 to 2019
$9.2M
Chromosome Metabolism and Cancer Training GrantT32CA009657 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI EISENMAN, ROBERT NEIL · 1991 to 2020
$7.6M
NCI NIH HHS T32 CA009657NCI NIH HHS T32 CA09657NIGMS NIH HHS R01 GM058465NIGMS NIH HHS R01GM058465
6 · The paper itself

Abstract

The S phase checkpoint response slows down replication in the presence of replication stress such that replication can resume normally once conditions are favorable. Both proper activation and deactivation of the checkpoint are crucial for genome stability. However, the mechanisms of checkpoint deactivation have been largely unknown. Here, we show that two highly conserved Saccharomyces cerevisiae ATP-dependent chromatin remodeling factors, Isw2 and Ino80, function to attenuate and deactivate S phase checkpoint activity. Genetic interactions revealed that these chromatin remodeling factors and the Rad53 phosphatases function in parallel in the DNA replication stress response. Following a transient replication stress, an isw2 nhp10 double mutant displays stronger and prolonged checkpoint activation without experiencing increased replication fork troubles. Isw2 and Ino80 are both enriched at stalled replication forks and physically and specifically interact with a single-stranded DNA binding protein, replication protein A (RPA). Based on these results, we propose that Isw2 and Ino80 are targeted to stalled replication forks via RPA and directly control the amplitude of S phase checkpoint activity and the subsequent deactivation process.

Indexed as

Chromatin Assembly and DisassemblyS Phase Cell Cycle CheckpointsAdenosine TriphosphatasesCell Cycle ProteinsCheckpoint Kinase 2DNA-Binding ProteinsDNA RepairDNA ReplicationHigh Mobility Group ProteinsProtein Serine-Threonine KinasesReplication OriginReplication Protein ASaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsStress, PhysiologicalTranscription FactorsAdenosine TriphosphatasesCell Cycle ProteinsCheckpoint Kinase 2DNA-Binding ProteinsHigh Mobility Group ProteinsINO80 complex, S cerevisiaeISWI proteinNHP10 protein, S cerevisiaeProtein Serine-Threonine KinasesRAD53 protein, S cerevisiaeReplication Protein ASaccharomyces cerevisiae ProteinsTranscription Factors

Identifiers

PMID21930788
PMCPMC3209248
OpenAlexW2167098320

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.