Evidence map›Paper›PMID 19965764›Full record

ArticleNucleic acids research2010

Elevated dNTP levels suppress hyper-recombination in Saccharomyces cerevisiae S-phase checkpoint mutants.

Michael Fasullo, Olga Tsaponina, Mingzeng Sun, Andrei Chabes

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

29 citing papers in PubMed, 44 citations in OpenAlex.

  1. bioRxiv : the preprint server for biology · 2025
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. DNA replication and mismatch repair safeguard against metabolic imbalances.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. dNTP pool levels modulate mutator phenotypes of error-prone DNA polymerase ε variants.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  19. Nucleotide salvage deficiencies, DNA damage and neurodegeneration.International journal of molecular sciences · 2015
    Review
  20. Article
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 3 institutions in 2 countries.

Michael FasulloOrdway Research Institute, 150 New Scotland Avenue, Albany, NY 12209, USA. mfasullo@ordwayresearch.org
Olga Tsaponina
Mingzeng Sun
Andrei Chabes
Albany State University · USAlbany Research Institute · USUmeå University · SE

Funding

RADIATION INDUCTION OF GENOMIC REARRANGEMENTS IN YEASTR01CA070105 · NCI · ORDWAY RESEARCH INSTITUTE, INC. · PI FASULLO, MICHAEL THOMAS · 2000 to 2004
$1.1M
RADIATION INDUCTION OF GENOMIC REARRANGEMENTS IN YEASTR29CA070105 · NCI · LOYOLA UNIVERSITY CHICAGO · PI FASULLO, MICHAEL THOMAS · 1995 to 1999
–
NCI NIH HHS CA70105
6 · The paper itself

Abstract

MEC1, the essential yeast homolog of the human ATR/ATM genes, controls the S-phase checkpoint and prevents replication fork collapse at slow zones of DNA replication. The viability of hypomorphic mec1-21 is reduced in the rad52 mutant, defective in homologous recombination, suggesting that replication generates recombinogenic lesions. We previously observed a 6-, 10- and 30-fold higher rate of spontaneous sister chromatid exchange (SCE), heteroallelic recombination and translocations, respectively, in mec1-21 mutants compared to wild-type. Here we report that the hyper-recombination phenotype correlates with lower deoxyribonucleoside triphosphate (dNTP) levels, compared to wild-type. By introducing a dun1 mutation, thus eliminating inducible expression of ribonucleotide reductase in mec1-21, rates of spontaneous SCE increased 15-fold above wild-type. All the hyper-recombination phenotypes were reduced by SML1 deletions, which increase dNTP levels. Measurements of dNTP pools indicated that, compared to wild-type, there was a significant decrease in dNTP levels in mec1-21, dun1 and mec1-21 dun1, while the dNTP levels of mec1-21 sml1, mec1-21 dun1 sml1 and sml1 mutants were approximately 2-fold higher. Interestingly, higher dNTP levels in mec1-21 dun1 sml1 correlate with approximately 2-fold higher rate of spontaneous mutagenesis, compared to mec1-21 dun1. We suggest that higher dNTP levels in specific checkpoint mutants suppress the formation of recombinogenic lesions.

Indexed as

Recombination, GeneticCell Cycle ProteinsDeoxyribonucleotidesIntracellular Signaling Peptides and ProteinsMutagenesisMutationProtein Serine-Threonine KinasesSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSister Chromatid ExchangeS PhaseTrefoil Factor-2Cell Cycle ProteinsDeoxyribonucleotidesDUN1 protein, S cerevisiaeIntracellular Signaling Peptides and ProteinsMEC1 protein, S cerevisiaeProtein Serine-Threonine KinasesSaccharomyces cerevisiae ProteinsSML1 protein, S cerevisiaeTFF2 protein, humanTrefoil Factor-2

Identifiers

PMID19965764
PMCPMC2831302
OpenAlexW2072152770

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.