Evidence map›Paper›PMID 10357828›Full record

ArticleThe EMBO journal1999

RAD53, DUN1 and PDS1 define two parallel G2/M checkpoint pathways in budding yeast.

R Gardner, C W Putnam, T Weinert

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed
5.6field-weighted citation impact, top 3% 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

79 citing papers in PubMed, 159 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Checkpoint Responses to DNA Double-Strand Breaks.Annual review of biochemistry · 2020
    Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. The yeast copper response is regulated by DNA damage.Molecular and cellular biology · 2013
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

19 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 1 institution in 1 country.

R GardnerDepartment of Molecular and Cellular Biology, The University of Arizona, PO Box 21016, Tucson, AZ 85721-0106, USA.
C W Putnam
T Weinert
University of Virginia · US

Funding

Integrative Cancer Scholars Training GrantT32CA009213 · NCI · UNIVERSITY OF ARIZONA · PI CAREW, JENNIFER S, CURIEL-LEWANDROWSKI, CLARA · 1985 to 2024
$8.6M
GENETIC CONTROL OF CELL CYCLE ARREST AFTER DNA DAMAGER01GM045276 · NIGMS · UNIVERSITY OF ARIZONA · PI WEINERT, TED A. · 1991 to 2000
$219k
MORPHOLOGIC SCREEN TO IDENTIFY G2/M CHECKPOINT GENESF33GM019370 · NIGMS · UNIVERSITY OF ARIZONA · PI PUTNAM, CHARLES W · 1998 to 1999
–
NCI NIH HHS CA 09213NIGMS NIH HHS GM 19370NIGMS NIH HHS GM 45276
6 · The paper itself

Abstract

Eukaryotic checkpoint genes regulate multiple cellular responses to DNA damage. In this report, we examine the roles of budding yeast genes involved in G2/M arrest and tolerance to UV exposure. A current model posits three gene classes: those encoding proteins acting on damaged DNA (e.g. RAD9 and RAD24), those transducing a signal (MEC1, RAD53 and DUN1) or those participating more directly in arrest (PDS1). Here, we define important features of the pathways subserved by those genes. MEC1, which we find is required for both establishment and maintenance of G2/M arrest, mediates this arrest through two parallel pathways. One pathway requires RAD53 and DUN1 (the 'RAD53 pathway'); the other pathway requires PDS1. Each pathway independently contributes approximately 50% to G2/M arrest, effects demonstrable after cdc13-induced damage or a double-stranded break inflicted by the HO endonuclease. Similarly, both pathways contribute independently to tolerance of UV irradiation. How the parallel pathways might interact ultimately to achieve arrest is not yet understood, but we do provide evidence that neither the RAD53 nor the PDS1 pathway appears to maintain arrest by inhibiting adaptation. Instead, we think it likely that both pathways contribute to establishing and maintaining arrest.

Indexed as

Cell CycleProtein Serine-Threonine KinasesSaccharomyces cerevisiae ProteinsAllelesCell Cycle ProteinsCheckpoint Kinase 2Cyclin BDeoxyribonucleases, Type II Site-SpecificDNA DamageEpistasis, GeneticFungal ProteinsGenes, cdcGenes, FungalIntracellular Signaling Peptides and ProteinsMitosisModels, BiologicalCell Cycle ProteinsCheckpoint Kinase 2Cyclin BDeoxyribonucleases, Type II Site-SpecificDUN1 protein, S cerevisiaeFungal ProteinsHO protein, S cerevisiaeIntracellular Signaling Peptides and ProteinsMEC1 protein, S cerevisiaeNuclear ProteinsPDS1 protein, S cerevisiaeProtein KinasesProtein Serine-Threonine KinasesRAD53 protein, S cerevisiaerad9 proteinSaccharomyces cerevisiae ProteinsSCEI protein, S cerevisiaeSecurin

Identifiers

PMID10357828
PMCPMC1171398
OpenAlexW1967834407

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.