Evidence map›Paper›PMID 19493358›Full record

ArticleBMC microbiology2009

Polymorphism and selection of rpoS in pathogenic Escherichia coli.

Tao Dong, Sarah M Chiang, Charlie Joyce, Rosemary Yu, Herb E Schellhorn

Abstract read
In one paragraph

Article in BMC microbiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

22 citing papers in PubMed.

  1. Article
  2. Article
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  4. RpoS contributes in a host-dependent manner toFrontiers in microbiology · 2022
    Article
  5. Article
  6. Effects of the Quinone Oxidoreductase WrbA onAntioxidants (Basel, Switzerland) · 2021
    Article
  7. Article
  8. Review
  9. Article
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  12. Article
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4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

5 authors.

Tao DongDepartment of Biology, Life Sciences Building, Rm, 433, McMaster University, 1280 Main Street West, Hamilton, ON, L8S 4K1, Canada. dongt2@mcmaster.ca
Sarah M Chiang
Charlie Joyce
Rosemary Yu
Herb E Schellhorn

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThough RpoS is important for survival of pathogenic Escherichia coli in natural environments, polymorphism in the rpoS gene is common. However, the causes of this polymorphism and consequential physiological effects on gene expression in pathogenic strains are not fully understood.

resultsIn this study, we found that growth on non-preferred carbon sources can efficiently select for loss of RpoS in seven of ten representative verocytotoxin-producing E. coli (VTEC) strains. Mutants (Suc++) forming large colonies on succinate were isolated at a frequency of 10-8 mutants per cell plated. Strain O157:H7 EDL933 yielded mainly mutants (about 90%) that were impaired in catalase expression, suggesting the loss of RpoS function. As expected, inactivating mutations in rpoS sequence were identified in these mutants. Expression of two pathogenicity-related phenotypes, cell adherence and RDAR (red dry and rough) morphotype, were also attenuated, indicating positive control by RpoS. For the other Suc++ mutants (10%) that were catalase positive, no mutation in rpoS was detected.

conclusionThe selection for loss of RpoS on poor carbon sources is also operant in most pathogenic strains, and thus is likely responsible for the occurrence of rpoS polymorphisms among E. coli isolates.

Indexed as

Polymorphism, GeneticBacterial ProteinsCell LineDNA, BacterialEscherichia coli ProteinsGene Expression Regulation, BacterialHumansMutagenesisPhenotypeSequence Analysis, DNASequence DeletionShiga-Toxigenic Escherichia coliSigma FactorSuccinic AcidVirulenceBacterial ProteinsDNA, BacterialEscherichia coli ProteinsSigma Factorsigma factor KatF protein, BacteriaSuccinic Acid

Identifiers

PMID19493358
PMCPMC2700278

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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.