Evidence map›Paper›PMID 18471973›Full record

ArticleMolecular cell2008

Colocalization of sensors is sufficient to activate the DNA damage checkpoint in the absence of damage.

Carla Yaneth Bonilla, Justine Amy Melo, David Paul Toczyski

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cell, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed
10.1field-weighted citation impact, top 1% 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

95 citing papers in PubMed, 164 citations in OpenAlex.

  1. Article
  2. Article
  3. DNA Damage and Replication Stress Checkpoints.Annual review of biochemistry · 2025
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. A DNA damage-induced phosphorylation circuit enhances Mec1Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  9. Article
  10. Review
  11. Review
  12. Novel insights into the mechanism of cell cycle kinases Mec1(ATR) and Tel1(ATM).Critical reviews in biochemistry and molecular biology · 2021
    Article
  13. Article
  14. Article
  15. Article
  16. Checkpoint Responses to DNA Double-Strand Breaks.Annual review of biochemistry · 2020
    Review
  17. Article
  18. Review
  19. Article
  20. Article

35 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

Carla Yaneth BonillaDepartment of Biochemistry and Biophysics, Cancer Research Institute, University of California, San Francisco, 2340 Sutter Street, San Francisco, CA 94115, USA.
Justine Amy Melo
David Paul Toczyski
University of California, San Francisco · USMassachusetts General Hospital · US

Funding

Maximizing Opportunities for Research Excellence - Evaluation Training SupplementR25GM056847 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI DUNCAN, D'ANNE S., SELLO, JASON K · 1998 to 2023
$14.1M
Regulation and Targets of the DNA Damage CheckpointR01GM059691 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI TOCZYSKI, DAVID PAUL · 1999 to 2015
$5.8M
NIGMS NIH HHS 1R25 GM56847NIGMS NIH HHS R01 GM059691NIGMS NIH HHS R25 GM056847PHS HHS 59691
6 · The paper itself

Abstract

Previous work on the DNA damage checkpoint in Saccharomyces cerevisiae has shown that two complexes independently sense DNA lesions: the kinase Mec1-Ddc2 and the PCNA-like 9-1-1 complex. To test whether colocalization of these components is sufficient for checkpoint activation, we fused these checkpoint proteins to the LacI repressor and artificially colocalized these fusions by expressing them in cells harboring Lac operator arrays. We observed Rad53 and Rad9 phosphorylation, Sml1 degradation, and metaphase delay, demonstrating that colocalization of these sensors is sufficient to activate the checkpoint in the absence of DNA damage. Our tethering system allowed us to establish that CDK functions in the checkpoint pathway downstream of damage processing and checkpoint protein recruitment. This CDK dependence is likely, at least in part, through Rad9, since mutation of CDK consensus sites compromised its checkpoint function.

Indexed as

DNA DamageGenes, cdcAdaptor Proteins, Signal TransducingAnimalsCell Cycle ProteinsCheckpoint Kinase 2ChromatinCyclin-Dependent KinasesEnzyme ActivationHistonesIntracellular Signaling Peptides and ProteinsMacromolecular SubstancesPhosphoproteinsProtein Serine-Threonine KinasesProtein SubunitsRecombinant Fusion ProteinsAdaptor Proteins, Signal TransducingCell Cycle ProteinsCheckpoint Kinase 2ChromatinCyclin-Dependent KinasesHistonesIntracellular Signaling Peptides and ProteinsLCD1 protein, S cerevisiaeMacromolecular SubstancesMEC1 protein, S cerevisiaePhosphoproteinsProtein Serine-Threonine KinasesProtein SubunitsRAD24 protein, S cerevisiaeRAD53 protein, S cerevisiaerad9 proteinRecombinant Fusion ProteinsRepressor ProteinsSaccharomyces cerevisiae Proteins

Identifiers

PMID18471973
PMCPMC2879338
OpenAlexW2030829729

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.