Evidence map›Paper›PMID 22651851›Full record

ArticleMolecular microbiology2012

Role of DNA base excision repair in the mutability and virulence of Streptococcus mutans.

Kaisha Gonzalez, Roberta C Faustoferri, Robert G Quivey

Abstract read
In one paragraph

Article in Molecular microbiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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

15 citing papers in PubMed.

  1. Article
  2. Genomic adaptation in group BbioRxiv : the preprint server for biology · 2025
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Streptococcus mutans: a new Gram-positive paradigm?Microbiology (Reading, England) · 2013
    Review
  14. Article
  15. 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.

Kaisha GonzalezDepartment of Microbiology and Immunology Center for Oral Biology, University of Rochester, Rochester, NY 14642, USA.
Roberta C Faustoferri
Robert G Quivey

Funding

Oxidative Stress Responses in Oral StreptococciR01DE013683 · NIDCR · UNIVERSITY OF ROCHESTER · PI QUIVEY, ROBERT G · 2000 to 2019
$6.2M
Training Program in Oral ScienceT90DE021985 · NIDCR · UNIVERSITY OF ROCHESTER · PI OVITT, CATHERINE, YULE, DAVID I · 2011 to 2021
$5.6M
Training Program in Oral Infectious DiseasesT32DE007165 · NIDCR · UNIVERSITY OF ROCHESTER · PI QUIVEY, ROBERT G · 1985 to 2005
$1.2M
NIDCR NIH HHS DE-13683NIDCR NIH HHS R01 DE013683NIDCR NIH HHS T32 DE007165NIDCR NIH HHS T32 DE-07165NIDCR NIH HHS T90 DE021985
6 · The paper itself

Abstract

The oral pathogen, Streptococcus mutans, possesses inducible DNA repair defences for protection against pH fluctuations and production of reactive oxygen metabolites such as hydrogen peroxide (H(2) O(2) ), which are present in the oral cavity. DNA base excision repair (BER) has a critical role in genome maintenance by preventing the accumulation of mutations associated with environmental factors and normal products of cellular metabolism. In this study, we examined the consequences of compromising the DNA glycosylases (Fpg and MutY) and endonucleases (Smx and Smn) of the BER pathway and their relative role in adaptation and virulence. Enzymatic characterization of the BER system showed that it protects the organism against the effects of the highly mutagenic lesion, 7,8-dihydro-8-oxo-2'-deoxyguanine (8-oxo-dG). S. mutans strains lacking a functional Fpg, MutY or Smn showed elevated spontaneous mutation frequencies; and, these mutator phenotypes correlated with the ability of the strains to survive killing by acid and oxidative agents. In addition, in the Galleria mellonella virulence model, strains of S. mutans deficient in Fpg, MutY and Smn showed increased virulence as compared with the parent strain. Our results suggest that, for S. mutans, mutator phenotypes, due to loss of BER enzymes, may confer an advantage to virulence of the organism.

Indexed as

DNA RepairAcidsAnimalsDNA, BacterialDNA Repair EnzymesGene DeletionLepidopteraMicrobial ViabilityOxidative StressStreptococcus mutansStress, PhysiologicalSurvival AnalysisVirulenceAcidsDNA, BacterialDNA Repair Enzymes

Identifiers

PMID22651851
PMCPMC3391326

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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.