Evidence map›Paper›PMID 26488727›Full record

ArticlePloS one2015

Acinetobacter baumannii Repeatedly Evolves a Hypermutator Phenotype in Response to Tigecycline That Effectively Surveys Evolutionary Trajectories to Resistance.

Troy G Hammerstrom, Kathryn Beabout, Thomas P Clements, Gerda Saxer, Yousif Shamoo

Abstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing 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

45 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. AdeABC, AdeFGH, and AdeIJK efflux pumps as key factors in tigecycline resistance of Acinetobacter baumannii: a study from Western Balkan hospitals.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2025
    Article
  5. Article
  6. Review
  7. Molecular mechanisms of tigecycline-resistance amongFrontiers in cellular and infection microbiology · 2024
    Review
  8. The tigecycline resistance mechanisms in Gram-negative bacilli.Frontiers in cellular and infection microbiology · 2024
    Review
  9. Frontiers in microbiology · 2024
    Review
  10. Review
  11. Article
  12. Antibiotics (Basel, Switzerland) · 2023
    Article
  13. Efflux-Related Carbapenem Resistance inInternational journal of molecular sciences · 2023
    Article
  14. Intracellular Experimental Evolution ofACS infectious diseases · 2023
    Article
  15. Article
  16. Resistance mechanisms of tigecycline inFrontiers in cellular and infection microbiology · 2023
    Review
  17. Article
  18. Review
  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

5 authors.

Troy G HammerstromDepartment of Biosciences, Rice University, Houston, Texas, United States of America.
Kathryn BeaboutDepartment of Biosciences, Rice University, Houston, Texas, United States of America.
Thomas P ClementsDepartment of Biosciences, Rice University, Houston, Texas, United States of America.
Gerda SaxerDepartment of Biosciences, Rice University, Houston, Texas, United States of America.
Yousif ShamooDepartment of Biosciences, Rice University, Houston, Texas, United States of America.

Funding

Defining Evolutionary Trajectories: Molecular adaptation to antibiotic resistanceR01AI080714 · NIAID · RICE UNIVERSITY · PI SHAMOO, YOUSIF · 2009 to 2023
$4.3M
Evolutionary Dynamics Leading to Tigecycline-Resistance in Enterococcus faecalis S613F31GM108402 · NIGMS · RICE UNIVERSITY · PI BEABOUT, KATHRYN ROBERTA · 2015 to 2015
$29k
NIAID NIH HHS R01 AI080714NIAID NIH HHS R01AI080714NIGMS NIH HHS F31 GM108402NIGMS NIH HHS F31GM108402
6 · The paper itself

Abstract

The evolution of hypermutators in response to antibiotic treatment in both clinical and laboratory settings provides a unique context for the study of adaptive evolution. With increased mutation rates, the number of hitchhiker mutations within an evolving hypermutator population is remarkably high and presents substantial challenges in determining which mutations are adaptive. Intriguingly however, hypermutators also provide an opportunity to explore deeply the accessible evolutionary trajectories that lead to increased organism fitness, in this case the evolution of antibiotic resistance to the clinically relevant antibiotic tigecycline by the hospital pathogen Acinetobacter baumannii. Using a continuous culture system, AB210M, a clinically derived strain of A. baumannii, was evolved to tigecycline resistance. Analysis of the adapted populations showed that nearly all the successful lineages became hypermutators via movement of a mobile element to inactivate mutS. In addition, metagenomic analysis of population samples revealed another 896 mutations that occurred at a frequency greater than 5% in the population, while 38 phenotypically distinct individual colonies harbored a total of 1712 mutations. These mutations were scattered throughout the genome and affected ~40% of the coding sequences. The most highly mutated gene was adeS, a known tigecycline-resistance gene; however, adeS was not solely responsible for the high level of TGC resistance. Sixteen other genes stood out as potentially relevant to increased resistance. The five most prominent candidate genes (adeS, rpsJ, rrf, msbA, and gna) consistently re-emerged in subsequent replicate population studies suggesting they are likely to play a role in adaptation to tigecycline. Interestingly, the repeated evolution of a hypermutator phenotype in response to antibiotic stress illustrates not only a highly adaptive strategy to resistance, but also a remarkably efficient survey of successful evolutionary trajectories.

Indexed as

Acinetobacter baumanniiAdaptation, PhysiologicalAnti-Bacterial AgentsBase SequenceDNA, BacterialDrug Resistance, BacterialEvolution, MolecularGenome, BacterialInterspersed Repetitive SequencesMicrobial Sensitivity TestsMinocyclineMutation RateMutS DNA Mismatch-Binding ProteinSequence Analysis, DNATigecyclineAnti-Bacterial AgentsDNA, BacterialMinocyclineMutS DNA Mismatch-Binding ProteinTigecycline

Identifiers

PMID26488727
PMCPMC4619398

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Registered trials

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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.