Evidence map›Paper›PMID 27091991›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2016

Antibiotic treatment enhances the genome-wide mutation rate of target cells.

Hongan Long, Samuel F Miller, Chloe Strauss, Chaoxian Zhao, Lei Cheng, Zhiqiang Ye, Katherine Griffin, Ronald Te, Heewook Lee, Chi-Chun Chen and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers.

0numbers the graph read from it
0cells of the map it votes in
115citing papers in PubMed
11.0field-weighted citation impact, top 1% 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

115 citing papers in PubMed, 218 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Extended sequence context shapes mutational bias inProceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  5. The unique role ofmBio · 2026
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Antibiotic-recalcitrant Salmonella during infection.Nature reviews. Microbiology · 2025
    Review
  11. Article
  12. Article
  13. Adaptive Resistance ofMicroorganisms · 2025
    Article
  14. Insights into antibiotic resistance promoted by quinolone exposure.Antimicrobial agents and chemotherapy · 2025
    Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article

55 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

11 authors at 3 institutions in 2 countries.

Hongan LongDepartment of Biology, Indiana University, Bloomington, IN 47405;
Samuel F MillerDepartment of Biology, Indiana University, Bloomington, IN 47405;
Chloe StraussDepartment of Biology, Indiana University, Bloomington, IN 47405;
Chaoxian ZhaoDepartment of Biology, School of Life Sciences, East China Normal University, Shanghai, China 200241;
Lei ChengHeilongjiang River Fisheries Research Institute, Chinese Academy of Fishery Sciences, Harbin, Heilongjiang Province, China 150001;
Zhiqiang YeDepartment of Biology, Indiana University, Bloomington, IN 47405;
Katherine GriffinDepartment of Biology, Indiana University, Bloomington, IN 47405;
Ronald TeDepartment of Biology, Indiana University, Bloomington, IN 47405;
Heewook LeeSchool of Informatics and Computing, Indiana University, Bloomington, IN 47405.
Chi-Chun ChenDepartment of Biology, Indiana University, Bloomington, IN 47405;
Michael LynchDepartment of Biology, Indiana University, Bloomington, IN 47405; milynch@indiana.edu.
Indiana University Bloomington · USChinese Academy of Fishery Sciences · CNEast China Normal University · CN

Funding

The Rate and Molecular Spectrum of Spontaneous MutationsR01GM036827 · NIGMS · UNIVERSITY OF OREGON · PI LYNCH, MICHAEL R · 1988 to 2016
$5.7M
NIGMS NIH HHS R01 GM036827
6 · The paper itself

Abstract

Although it is well known that microbial populations can respond adaptively to challenges from antibiotics, empirical difficulties in distinguishing the roles of de novo mutation and natural selection have left several issues unresolved. Here, we explore the mutational properties of Escherichia coli exposed to long-term sublethal levels of the antibiotic norfloxacin, using a mutation accumulation design combined with whole-genome sequencing of replicate lines. The genome-wide mutation rate significantly increases with norfloxacin concentration. This response is associated with enhanced expression of error-prone DNA polymerases and may also involve indirect effects of norfloxacin on DNA mismatch and oxidative-damage repair. Moreover, we find that acquisition of antibiotic resistance can be enhanced solely by accelerated mutagenesis, i.e., without direct involvement of selection. Our results suggest that antibiotics may generally enhance the mutation rates of target cells, thereby accelerating the rate of adaptation not only to the antibiotic itself but to additional challenges faced by invasive pathogens.

Indexed as

Anti-Bacterial AgentsDNA DamageDNA RepairDose-Response Relationship, DrugEscherichia coliEvolution, MolecularGenome, BacterialGenomic InstabilityMutagenesisMutationNorfloxacinAnti-Bacterial AgentsNorfloxacinantibiotic resistanceDNA repairlow-fidelity polymerasesmutation rateresistance evolution

Identifiers

PMID27091991
PMCPMC4983809
OpenAlexW2337745053

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.