Evidence map›Paper›PMID 26460006›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2015

Determinants of spontaneous mutation in the bacterium Escherichia coli as revealed by whole-genome sequencing.

Patricia L Foster, Heewook Lee, Ellen Popodi, Jesse P Townes, Haixu Tang

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers.

0numbers the graph read from it
0cells of the map it votes in
117citing 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

117 citing papers in PubMed.

  1. Article
  2. Article
  3. Translation accuracy in E. coli.Nucleic acids research · 2026
    Article
  4. Article
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  6. Extended sequence context shapes mutational bias inProceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  7. Article
  8. Article
  9. Article
  10. Detection of mutations: from Ames test to duplex sequencing.Frontiers in molecular biosciences · 2026
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

57 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

5 authors.

Patricia L FosterDepartment of Biology, Indiana University, Bloomington, IN 47405; plfoster@indiana.edu.
Heewook LeeSchool of Informatics and Computing, Indiana University, Bloomington, IN 47405.
Ellen PopodiDepartment of Biology, Indiana University, Bloomington, IN 47405;
Jesse P TownesDepartment of Biology, Indiana University, Bloomington, IN 47405;
Haixu TangSchool of Informatics and Computing, Indiana University, Bloomington, IN 47405.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A complete understanding of evolutionary processes requires that factors determining spontaneous mutation rates and spectra be identified and characterized. Using mutation accumulation followed by whole-genome sequencing, we found that the mutation rates of three widely diverged commensal Escherichia coli strains differ only by about 50%, suggesting that a rate of 1-2 × 10(-3) mutations per generation per genome is common for this bacterium. Four major forces are postulated to contribute to spontaneous mutations: intrinsic DNA polymerase errors, endogenously induced DNA damage, DNA damage caused by exogenous agents, and the activities of error-prone polymerases. To determine the relative importance of these factors, we studied 11 strains, each defective for a major DNA repair pathway. The striking result was that only loss of the ability to prevent or repair oxidative DNA damage significantly impacted mutation rates or spectra. These results suggest that, with the exception of oxidative damage, endogenously induced DNA damage does not perturb the overall accuracy of DNA replication in normally growing cells and that repair pathways may exist primarily to defend against exogenously induced DNA damage. The thousands of mutations caused by oxidative damage recovered across the entire genome revealed strong local-sequence biases of these mutations. Specifically, we found that the identity of the 3' base can affect the mutability of a purine by oxidative damage by as much as eightfold.

Indexed as

Genes, BacterialMutationAlkylationDNA RepairEscherichia coliDNA repairevolutionmutation accumulationmutation rateoxidative DNA damage

Identifiers

PMID26460006
PMCPMC4640725

What OpenQuestion holds

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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.