Evidence map›Paper›PMID 19019142›Full record

ArticleMolecular microbiology2009

DNA polymerase switching: effects on spontaneous mutagenesis in Escherichia coli.

Elena Curti, John P McDonald, Samantha Mead, Roger Woodgate

Open access · bronzeAbstract read
In one paragraph

Article in Molecular microbiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

36 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. SetRDNA repair · 2019
    Article
  11. Article
  12. Sources of spontaneous mutagenesis in bacteria.Critical reviews in biochemistry and molecular biology · 2018
    Review
  13. Article
  14. Antibiotic treatment enhances the genome-wide mutation rate of target cells.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  15. Article
  16. Determinants of spontaneous mutation in the bacterium Escherichia coli as revealed by whole-genome sequencing.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  17. Article
  18. Hypermutability and error catastrophe due to defects in ribonucleotide reductase.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  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

4 authors at 1 institution in 1 country.

Elena CurtiLaboratory of Genomic Integrity, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892-3371, USA.
John P McDonald
Samantha Mead
Roger Woodgate
National Institutes of Health · US

Funding

DNA Replication, Repair, and Mutagenesis In Eukaryotic And Prokaryotic CellsZIAHD001500 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI WOODGATE, ROGER · 2009 to 2025
$37.5M
DNA REPLICATION, REPAIR, AND MUTAGENESIS IN EUKARYOTIC AND PROKARYOTIC CELLSZ01HD001500 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI WOODGATE, ROGER · 1985 to 2008
$3.1M
Intramural NIH HHS
6 · The paper itself

Abstract

Escherichia coli possesses five known DNA polymerases (pols). Pol III holoenzyme is the cell's main replicase, while pol I is responsible for the maturation of Okazaki fragments and filling gaps generated during nucleotide excision repair. Pols II, IV and V are significantly upregulated as part of the cell's global SOS response to DNA damage and under these conditions, may alter the fidelity of DNA replication by potentially interfering with the ability of pols I and III to complete their cellular functions. To test this hypothesis, we determined the spectrum of rpoB mutations arising in an isogenic set of mutL strains differentially expressing the chromosomally encoded pols. Interestingly, mutagenic hot spots in rpoB were identified that are susceptible to the actions of pols I-V. For example, in a recA730 lexA(Def) mutL background most transversions were dependent upon pols IV and V. In contrast, transitions were largely dependent upon pol I and to a lesser extent, pol III. Furthermore, the extent of pol I-dependent mutagenesis at one particular site was modulated by pols II and IV. Our observations suggest that there is considerable interplay among all five E. coli polymerases that either reduces or enhances the mutagenic load on the E. coli chromosome.

Indexed as

MutagenesisDNA-Directed DNA PolymeraseEscherichia coliEscherichia coli ProteinsMutation, MissenseDNA-Directed DNA PolymeraseEscherichia coli Proteins

Identifiers

PMID19019142
PMCPMC2680738
OpenAlexW2004007263

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.