Evidence map›Paper›PMID 17220404›Full record

ArticleAntimicrobial agents and chemotherapy2007

Increased genome instability in Escherichia coli lon mutants: relation to emergence of multiple-antibiotic-resistant (Mar) mutants caused by insertion sequence elements and large tandem genomic amplifications.

Hervé Nicoloff, Vincent Perreten, Stuart B Levy

Open access · greenAbstract read
In one paragraph

Article in Antimicrobial agents and chemotherapy, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.2field-weighted citation impact, top 24% 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

32 citing papers in PubMed, 56 citations in OpenAlex.

  1. Lon protease-mediated secretome profiling inMicrobiology resource announcements · 2026
    Article
  2. Article
  3. Insights into antibiotic resistance promoted by quinolone exposure.Antimicrobial agents and chemotherapy · 2025
    Article
  4. ISmBio · 2024
    Article
  5. Suppression of theRNA (New York, N.Y.) · 2024
    Article
  6. The induced and intrinsic resistance ofMicrobiology spectrum · 2024
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Emergence of tigecycline resistance inInfection and drug resistance · 2018
    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

3 authors at 1 institution in 2 countries.

Hervé NicoloffCenter for Adaptation Genetics and Drug Resistance, Department of Molecular Biology and Microbiology, Tufts University School of Medicine, 136 Harrison Ave., Boston, MA 02111, USA.
Vincent Perreten
Stuart B Levy
CNR de la Résistance aux Antibiotiques · FR

Funding

The multiple antibiotic resistance (MAR)regulonR01AI056021 · NIAID · TUFTS UNIVERSITY BOSTON · PI LEVY, STUART B. · 2003 to 2017
$8.9M
NIAID NIH HHS AI56021NIAID NIH HHS R01 AI056021
6 · The paper itself

Abstract

Thirteen spontaneous multiple-antibiotic-resistant (Mar) mutants of Escherichia coli AG100 were isolated on Luria-Bertani (LB) agar in the presence of tetracycline (4 microg/ml). The phenotype was linked to insertion sequence (IS) insertions in marR or acrR or unstable large tandem genomic amplifications which included acrAB and which were bordered by IS3 or IS5 sequences. Five different lon mutations, not related to the Mar phenotype, were also found in 12 of the 13 mutants. Under specific selective conditions, most drug-resistant mutants appearing late on the selective plates evolved from a subpopulation of AG100 with lon mutations. That the lon locus was involved in the evolution to low levels of multidrug resistance was supported by the following findings: (i) AG100 grown in LB broth had an important spontaneous subpopulation (about 3.7x10(-4)) of lon::IS186 mutants, (ii) new lon mutants appeared during the selection on antibiotic-containing agar plates, (iii) lon mutants could slowly grow in the presence of low amounts (about 2x MIC of the wild type) of chloramphenicol or tetracycline, and (iv) a lon mutation conferred a mutator phenotype which increased IS transposition and genome rearrangements. The association between lon mutations and mutations causing the Mar phenotype was dependent on the medium (LB versus MacConkey medium) and the antibiotic used for the selection. A previously reported unstable amplifiable high-level resistance observed after the prolonged growth of Mar mutants in a low concentration of tetracycline or chloramphenicol can be explained by genomic amplification.

Indexed as

Genome, BacterialGenomic InstabilityAnti-Bacterial AgentsATP-Binding Cassette, Sub-Family C ProteinsDNA, BacterialDNA-Binding ProteinsDNA Transposable ElementsDrug Resistance, Multiple, BacterialEscherichia coliEscherichia coli ProteinsGene AmplificationMutationProtease LaAnti-Bacterial AgentsATP-Binding Cassette, Sub-Family C ProteinsDNA, BacterialDNA-Binding ProteinsDNA Transposable ElementsEscherichia coli ProteinsLon protein, E coliMarA protein, E coliProtease La

Identifiers

PMID17220404
PMCPMC1855481
OpenAlexW2126887640

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.