Evidence map›Paper›PMID 19635811›Full record

ArticleMolecular and cellular biology2009

The polymerase eta translesion synthesis DNA polymerase acts independently of the mismatch repair system to limit mutagenesis caused by 7,8-dihydro-8-oxoguanine in yeast.

Sarah V Mudrak, Caroline Welz-Voegele, Sue Jinks-Robertson

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2009. 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
0.5field-weighted citation impact, top 33% 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, 28 citations in OpenAlex.

  1. Article
  2. 8-Oxoadenine: A «New» Player of the Oxidative Stress in Mammals?International journal of molecular sciences · 2024
    Review
  3. Article
  4. Article
  5. Genetic Control of Oxidative Mutagenesis inJournal of bacteriology · 2020
    Article
  6. Mechanisms of genome evolution in Candida albicans.Current opinion in microbiology · 2019
    Review
  7. Article
  8. Article
  9. Global analysis of mutations driving microevolution of a heterozygous diploid fungal pathogen.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. In vivo bypass of 8-oxodG.PLoS genetics · 2013
    Article
  16. Review
  17. 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

3 authors at 2 institutions in 2 countries.

Sarah V MudrakDepartment of Molecular Genetics and Microbiology, DUMC Box 3020, Duke University Medical Center, Durham, NC 27710, USA.
Caroline Welz-Voegele
Sue Jinks-Robertson
Duke Medical Center · USDuke University · US

Funding

REGULATION OF MITOTIC RECOMBINATION IN YEASTR01GM038464 · NIGMS · EMORY UNIVERSITY · PI JINKS-ROBERTSON, SUE · 1992 to 2015
$3.6M
Tolerance of spontaneous and induced DNA damage in yeastR01GM064769 · NIGMS · EMORY UNIVERSITY · PI JINKS-ROBERTSON, SUE · 2002 to 2010
$1.9M
RECOMBINATION BETWEEN REPEATED SEQUENCE IN YEASTR29GM038464 · NIGMS · EMORY UNIVERSITY · PI JINKS-ROBERTSON, SUE · 1987 to 1991
–
NIGMS NIH HHS GM038464NIGMS NIH HHS GM064769NIGMS NIH HHS R01 GM038464NIGMS NIH HHS R01 GM064769
6 · The paper itself

Abstract

Reactive oxygen species are ubiquitous mutagens that have been linked to both disease and aging. The most studied oxidative lesion is 7,8-dihydro-8-oxoguanine (GO), which is often miscoded during DNA replication, resulting specifically in GC --> TA transversions. In yeast, the mismatch repair (MMR) system repairs GO.A mismatches generated during DNA replication, and the polymerase eta (Poleta) translesion synthesis DNA polymerase additionally promotes error-free bypass of GO lesions. It has been suggested that Poleta limits GO-associated mutagenesis exclusively through its participation in the filling of MMR-generated gaps that contain GO lesions. In the experiments reported here, the SUP4-o forward-mutation assay was used to monitor GC --> TA mutation rates in strains defective in MMR (Msh2 or Msh6) and/or in Poleta activity. The results clearly demonstrate that Poleta can function independently of the MMR system to prevent GO-associated mutations, presumably through preferential insertion of cytosine opposite replication-blocking GO lesions. Furthermore, the Poleta-dependent bypass of GO lesions is more efficient on the lagging strand of replication and requires an interaction with proliferating cell nuclear antigen. These studies establish a new paradigm for the prevention of GO-associated mutagenesis in eukaryotes.

Indexed as

DNA Mismatch RepairMutagenesisAllelesDNA-Directed DNA PolymeraseDNA, FungalDNA ReplicationGenome, FungalGuanineSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsY-Family DNA Polymerases7,8-dihydro-8-oxoguanineDNA-Directed DNA PolymeraseDNA, FungalGuanineRad30 proteinSaccharomyces cerevisiae ProteinsY-Family DNA Polymerases

Identifiers

PMID19635811
PMCPMC2747974
OpenAlexW2119692351

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.