Evidence map›Paper›PMID 19841096›Full record

ArticleGenetics2010

Participation of DNA polymerase zeta in replication of undamaged DNA in Saccharomyces cerevisiae.

Matthew R Northam, Heather A Robinson, Olga V Kochenova, Polina V Shcherbakova

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

76 citing papers in PubMed, 107 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. CRISPR/Cas9 as a Mutagenic Factor.International journal of molecular sciences · 2024
    Review
  6. Article
  7. Article
  8. Review
  9. Global genomic instability caused by reduced expression of DNA polymerase ε in yeast.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. DNA polymerase δ proofreads errors made by DNA polymerase ε.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article

16 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 2 institutions in 1 country.

Matthew R NorthamEppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, Nebraska 68198, USA.
Heather A Robinson
Olga V Kochenova
Polina V Shcherbakova
University of Nebraska Medical Center · USNebraska Medical Center · US

Funding

Translesion Synthesis DNA Polymerases and Genome InstabilityR01ES015869 · NIEHS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI SHCHERBAKOVA, POLINA V · 2009 to 2023
$4.7M
Role of DNA polymerases in chromosome stability controlK22ES011644 · NIEHS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI SHCHERBAKOVA, POLINA V · 2003 to 2005
$321k
NIEHS NIH HHS ES011644NIEHS NIH HHS ES015869NIEHS NIH HHS K22 ES011644NIEHS NIH HHS R01 ES015869
6 · The paper itself

Abstract

Translesion synthesis DNA polymerases contribute to DNA damage tolerance by mediating replication of damaged templates. Due to the low fidelity of these enzymes, lesion bypass is often mutagenic. We have previously shown that, in Saccharomyces cerevisiae, the contribution of the error-prone DNA polymerase zeta (Polzeta) to replication and mutagenesis is greatly enhanced if the normal replisome is defective due to mutations in replication genes. Here we present evidence that this defective-replisome-induced mutagenesis (DRIM) results from the participation of Polzeta in the copying of undamaged DNA rather than from mutagenic lesion bypass. First, DRIM is not elevated in strains that have a high level of endogenous DNA lesions due to defects in nucleotide excision repair or base excision repair pathways. Second, DRIM remains unchanged when the level of endogenous oxidative DNA damage is decreased by using anaerobic growth conditions. Third, analysis of the spectrum of mutations occurring during DRIM reveals the characteristic error signature seen during replication of undamaged DNA by Polzeta in vitro. These results extend earlier findings in Escherichia coli indicating that Y-family DNA polymerases can contribute to the copying of undamaged DNA. We also show that exposure of wild-type yeast cells to the replication inhibitor hydroxyurea causes a Polzeta-dependent increase in mutagenesis. This suggests that DRIM represents a response to replication impediment per se rather than to specific defects in the replisome components.

Indexed as

DNA ReplicationBase SequenceDNA DamageDNA-Directed DNA PolymeraseDNA, FungalHydroxyureaMolecular Sequence DataMultienzyme ComplexesMutagenesisMutationOxidative StressReplisomesSaccharomyces cerevisiaeDNA-Directed DNA PolymeraseDNA, FungalDNA polymerase zetaHydroxyureaMultienzyme ComplexesReplisomes

Identifiers

PMID19841096
PMCPMC2815923
OpenAlexW2148123849

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.