Evidence map›Paper›PMID 17689152›Full record

ArticleDNA repair2007

Analysis of Rev1p and Pol zeta in mitochondrial mutagenesis suggests an alternative pathway of damage tolerance.

Lidza Kalifa, Elaine A Sia

Open access · greenAbstract read
In one paragraph

Article in DNA repair, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

23 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Translesion DNA polymerases in eukaryotes: what makes them tick?Critical reviews in biochemistry and molecular biology · 2017
    Review
  6. Article
  7. Mitochondrial DNA replication: a PrimPol perspective.Biochemical Society transactions · 2017
    Review
  8. DNA polymerases in the mitochondria: A critical review of the evidence.Frontiers in bioscience (Landmark edition) · 2017
    Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  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

2 authors at 1 institution in 1 country.

Lidza KalifaDepartment of Biology, University of Rochester, Rochester, NY 14627, United States.
Elaine A Sia
University of Rochester · US

Funding

DNA Repair and Mutagenesis in S cerevisiaeR01GM063626 · NIGMS · UNIVERSITY OF ROCHESTER · PI SIA, ELAINE A · 2001 to 2005
$1.3M
NIGMS NIH HHS GM63626NIGMS NIH HHS R01 GM063626
6 · The paper itself

Abstract

Ultraviolet light is a potent DNA damaging agent that induces bulky lesions in DNA which block the replicative polymerases. In order to ensure continued DNA replication and cell viability, specialized translesion polymerases bypass these lesions at the expense of introducing mutations in the nascent DNA strand. A recent study has shown that the N-terminal sequences of the nuclear translesion polymerases Rev1p and Pol zeta can direct GFP to the mitochondrial compartment of Saccharomyces cerevisiae. We have investigated the role of these polymerases in mitochondrial mutagenesis. Our analysis of mitochondrial DNA point mutations, microsatellite instability, and the spectra of mitochondrial mutations indicate that these translesion polymerases function in a less mutagenic pathway in the mitochondrial compartment than they do in the nucleus. Mitochondrial phenotypes resulting from the loss of Rev1p and Pol zeta suggest that although these polymerases are responsible for the majority of mitochondrial frameshift mutations, they do not greatly contribute to mitochondrial DNA point mutations. Analysis of spontaneous mitochondrial DNA point mutations suggests that Pol zeta may play a role in general mitochondrial DNA maintenance. In addition, we observe a 20-fold increase in UV-induced mitochondrial DNA point mutations in rev deficient strains. Our data provides evidence for an alternative damage tolerance pathway that is specific to the mitochondrial compartment.

Indexed as

DNA DamagePoint MutationDNA-Directed DNA PolymeraseDNA, FungalDNA ReplicationNucleotidyltransferasesSaccharomyces cerevisiae ProteinsUltraviolet RaysY-Family DNA PolymerasesDNA-Directed DNA PolymeraseDNA, FungalDNA polymerase zetaNucleotidyltransferasesREV1 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsY-Family DNA Polymerases

Identifiers

PMID17689152
PMCPMC2129123
OpenAlexW2020118122

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.