Evidence map›Paper›PMID 20128927›Full record

ArticleBMC microbiology2010

Escherichia coli genes that reduce the lethal effects of stress.

Xiulin Han, Angella Dorsey-Oresto, Muhammad Malik, Jian-Ying Wang, Karl Drlica, Xilin Zhao, Tao Lu

Open access · goldAbstract read
In one paragraph

Article in BMC microbiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
5.1field-weighted citation impact, top 5% 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

29 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Genome-wide Screening of the Escherichia coli Keio Knockout Collection Identifies Genetic Determinants of Epetraborole Hypersusceptibility.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2025
    Article
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  4. Review
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  6. Evolution of antimicrobial resistance inFrontiers in microbiology · 2023
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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

7 authors at 2 institutions in 1 country.

Xiulin HanYunnan Institute of Microbiology, Yunnan University, 52 Cui Hu Bei Lu, Kunming, Yunnan 650091, PR China.
Angella Dorsey-Oresto
Muhammad Malik
Jian-Ying Wang
Karl Drlica
Xilin Zhao
Tao Lu
Rutgers New Jersey Medical SchoolYunnan University · CN

Funding

Novel fluoroquinolones for killing dormant Mycobacterium tuberculosisR01AI073491 · NIAID · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI DRLICA, KARL A, KERNS, ROBERT JOHN · 2007 to 2015
$5.1M
DNA GYRASE AND QUINOLONE RESISTANCE IN TUBERCULOSISR01AI035257 · NIAID · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI DRLICA, KARL A · 1993 to 2007
$4.3M
New genes involved in cellular responses to quinolone treatmentR21AI068014 · NIAID · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI ZHAO, XILIN · 2007 to 2008
$425k
NIAID NIH HHS AI068014NIAID NIH HHS AI 073491NIAID NIH HHS AI35257NIAID NIH HHS R01 AI035257NIAID NIH HHS R01 AI073491NIAID NIH HHS R21 AI068014
6 · The paper itself

Abstract

backgroundThe continuing emergence of antimicrobial resistance requires the development of new compounds and/or enhancers of existing compounds. Genes that protect against the lethal effects of antibiotic stress are potential targets of enhancers. To distinguish such genes from those involved in drug uptake and efflux, a new susceptibility screen is required.

resultsTransposon (Tn5)-mediated mutagenesis was used to create a library of Escherichia coli mutants that was screened for hypersensitivity to the lethal action of quinolones and counter-screened to have wild-type bacteriostatic susceptibility. Mutants with this novel "hyperlethal" phenotype were found. The phenotype was transferable to other E. coli strains by P1-mediated transduction, and for a subset of the mutants the phenotype was complemented by the corresponding wild-type gene cloned into a plasmid. Thus, the inactivation of these genes was responsible for hyperlethality. Nucleotide sequence analysis identified 14 genes, mostly of unknown function, as potential factors protecting from lethal effects of stress. The 14 mutants were killed more readily than wild-type cells by mitomycin C and hydrogen peroxide; nine were also more readily killed by UV irradiation, and several exhibited increased susceptibility to killing by sodium dodecyl sulfate. No mutant was more readily killed by high temperature.

conclusionsA new screening strategy identified a diverse set of E. coli genes involved in the response to lethal antimicrobial and environmental stress, with some genes being involved in the response to multiple stressors. The gene set, which differed from sets previously identified with bacteriostatic assays, provides an entry point for obtaining small-molecule enhancers that will affect multiple antimicrobial agents.

Indexed as

Anti-Bacterial AgentsDNA, BacterialDrug Resistance, BacterialEscherichia coliGene Expression Regulation, BacterialGene LibraryGenes, BacterialGenetic Complementation TestHot TemperatureHydrogen-Ion ConcentrationHydrogen PeroxideMicrobial Sensitivity TestsMutagenesis, InsertionalNalidixic AcidPhenotypeSequence Analysis, DNAAnti-Bacterial AgentsDNA, BacterialHydrogen PeroxideNalidixic Acid

Identifiers

PMID20128927
PMCPMC2824699
OpenAlexW2069967265

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.