Evidence map›Paper›PMID 7828811›Full record

ArticleGenetics1994

Characterization of G1 checkpoint control in the yeast Saccharomyces cerevisiae following exposure to DNA-damaging agents.

W Siede, A S Friedberg, I Dianova, E C Friedberg

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Genetics, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
5.9field-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

66 citing papers in PubMed, 148 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Checkpoint Responses to DNA Double-Strand Breaks.Annual review of biochemistry · 2020
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Induction of a G1-S checkpoint in fission yeast.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Article
  11. Review
  12. Article
  13. Article
  14. UV irradiation induces a postreplication DNA damage checkpoint.Proceedings of the National Academy of Sciences of the United States of America · 2006
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Intra-G1 arrest in response to UV irradiation in fission yeast.Proceedings of the National Academy of Sciences of the United States of America · 2003
    Article
  20. Article

6 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

4 authors at 1 institution in 1 country.

W SiedeDepartment of Pathology, University of Texas Southwestern Medical Center, Dallas 75235.
A S Friedberg
I Dianova
E C Friedberg
The University of Texas Southwestern Medical Center · US

Funding

DNA REPAIR AND ITS RELATIONSHIP TO CARCINOGENESISR01CA012428 · NCI · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI FRIEDBERG, ERROL · 1985 to 2001
$633k
DNA REPAIR AND ITS RELATIONSHIP TO CARCINOGENESISR37CA012428 · NCI · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI FRIEDBERG, ERROL · 1989 to 1996
–
NCI NIH HHS CA12428
6 · The paper itself

Abstract

The delay of S-phase following treatment of yeast cells with DNA-damaging agents is an actively regulated response that requires functional RAD9 and RAD24 genes. An analysis of cell cycle arrest indicates the existence of (at least) two checkpoints for damaged DNA prior to S-phase; one at START (a G1 checkpoint characterized by pheromone sensitivity of arrested cells) and one between the CDC4- and CDC7-mediated steps (termed the G1/S checkpoint). When a dna1-1 mutant (that affects early events of replicon initiation) also carries a rad9 deletion mutation, it manifests a failure to arrest in G1/S following incubation at the restrictive temperature. This failure to execute regulated G1/S arrest is correlated with enhanced thermosensitivity of colony-forming ability. In an attempt to characterize the signal for RAD9 gene-dependent G1 and G1/S cell cycle arrest, we examined the influence of the continued presence of unexcised photoproducts. In mutants defective in nucleotide excision repair, cessation of S-phase was observed at much lower doses of UV radiation compared to excision-proficient cells. However, this response was not RAD9-dependent. We suggest that an intermediate of nucleotide excision repair, such as DNA strand breaks or single-stranded DNA tracts, is required to activate RAD9-dependent G1 and G1/S checkpoint controls.

Indexed as

Cell Cycle ProteinsDNA-Binding ProteinsDNA DamageEndodeoxyribonucleasesPeptidesSaccharomyces cerevisiae ProteinsCell CycleFlow CytometryFungal ProteinsG1 PhaseGene DeletionGenes, FungalGenotypeIntracellular Signaling Peptides and ProteinsMating FactorPeptide BiosynthesisCell Cycle ProteinsDNA-Binding ProteinsEndodeoxyribonucleasesFungal ProteinsIntracellular Signaling Peptides and ProteinsMating FactorPeptidesPheromonesRAD24 protein, S cerevisiaeRAD2 protein, S cerevisiaerad9 proteinSaccharomyces cerevisiae Proteins

Identifiers

PMID7828811
PMCPMC1206146
OpenAlexW2140771227

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.