Evidence map›Paper›PMID 23204459›Full record

ArticleJournal of bacteriology2013

Evolution in fast forward: a potential role for mutators in accelerating Staphylococcus aureus pathoadaptation.

Gregory S Canfield, Johanna M Schwingel, Matthew H Foley, Kelly L Vore, Kanitsak Boonanantanasarn, Ann L Gill, Mark D Sutton, Steven R Gill

Open access · bronzeAbstract read
In one paragraph

Article in Journal of bacteriology, 2013. 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
0.8field-weighted citation impact, top 29% 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, 38 citations in OpenAlex.

  1. Base excision repair inFrontiers in microbiology · 2026
    Review
  2. Phylogenetic analysis ofOpen veterinary journal · 2024
    Article
  3. Microbiota and metabolic adaptation shapebioRxiv : the preprint server for biology · 2024
    Article
  4. Article
  5. Frontiers in microbiology · 2021
    Article
  6. Article
  7. Article
  8. Inhibitors of DNA Glycosylases as Prospective Drugs.International journal of molecular sciences · 2020
    Review
  9. TheGenes · 2020
    Article
  10. Article
  11. Staphylococci: Evolving Genomes.Microbiology spectrum · 2019
    Review
  12. Article
  13. The Response ofJournal of bacteriology · 2019
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. 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

8 authors at 2 institutions in 1 country.

Gregory S CanfieldDepartment of Microbiology and Immunology, University of Rochester School of Medicine and Dentistry, Rochester, New York, USA.
Johanna M Schwingel
Matthew H Foley
Kelly L Vore
Kanitsak Boonanantanasarn
Ann L Gill
Mark D Sutton
Steven R Gill
University of Rochester · USUniversity at Buffalo, State University of New York · US

Funding

Training Program in Oral ScienceT90DE021985 · NIDCR · UNIVERSITY OF ROCHESTER · PI OVITT, CATHERINE, YULE, DAVID I · 2011 to 2021
$5.6M
Virulence Determinants in Staphylococcus BacteremiaR01AI059111 · NIAID · UNIVERSITY OF ROCHESTER · PI GILL, STEVEN R. · 2004 to 2012
$3.4M
NIAID NIH HHS R01 AI059111NIDCR NIH HHS T90 DE021985
6 · The paper itself

Abstract

Pathogen evolution and subsequent phenotypic heterogeneity during chronic infection are proposed to enhance Staphylococcus aureus survival during human infection. We tested this theory by genetically and phenotypically characterizing strains with mutations constructed in the mismatch repair (MMR) and oxidized guanine (GO) system, termed mutators, which exhibit increased spontaneous-mutation frequencies. Analysis of these mutators revealed not only strain-dependent increases in the spontaneous-mutation frequency but also shifts in mutational type and hot spots consistent with loss of GO or MMR functions. Although the GO and MMR systems are relied upon in some bacterial species to prevent reactive oxygen species-induced DNA damage, no deficit in hydrogen peroxide sensitivity was found when either of these DNA repair pathways was lost in S. aureus. To gain insight into the contribution of increased mutation supply to S. aureus pathoadaptation, we measured the rate of α-hemolysin and staphyloxanthin inactivation during serial passage. Detection of increased rates of α-hemolysin and staphyloxanthin inactivation in GO and MMR mutants suggests that these strains are capable of modifying virulence phenotypes implicated in mediating infection. Accelerated derivation of altered virulence phenotypes, combined with the absence of increased ROS sensitivity, highlights the potential of mutators to drive pathoadaptation in the host and serve as catalysts for persistent infections.

Indexed as

MutationAdaptation, PhysiologicalBacterial ToxinsBase SequenceDNA, BacterialDNA DamageDNA Mismatch RepairGene Expression Regulation, BacterialGuanineHemolysin ProteinsHydrogen PeroxideMolecular Sequence DataOxidation-ReductionReactive Oxygen SpeciesStaphylococcus aureusTime FactorsBacterial ToxinsDNA, BacterialGuanineHemolysin ProteinsHydrogen PeroxideReactive Oxygen Speciesstaphylococcal alpha-toxinstaphyloxanthinVirulence FactorsXanthophylls

Identifiers

PMID23204459
PMCPMC3554003
OpenAlexW2056254121

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.