Evidence map›Paper›PMID 26904510›Full record

ArticleFrontiers in cellular and infection microbiology2016

The Two-Component System CpxRA Negatively Regulates the Locus of Enterocyte Effacement of Enterohemorrhagic Escherichia coli Involving σ(32) and Lon protease.

Miguel A De la Cruz, Jason K Morgan, Miguel A Ares, Jorge A Yáñez-Santos, James T Riordan, Jorge A Girón

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Frontiers in cellular and infection microbiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
5.8field-weighted citation impact, top 4% 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

23 citing papers in PubMed, 39 citations in OpenAlex.

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  8. Simulated Colonic Fluid Replicates theInfection and immunity · 2022
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  15. Review
  16. The Interaction ofFrontiers in cellular and infection microbiology · 2019
    Article
  17. Review
  18. The Coli Surface Antigen CS3 of EnterotoxigenicFrontiers in microbiology · 2019
    Article
  19. Review
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 2 countries.

Miguel A De la CruzUnidad de Investigación Médica en Enfermedades Infecciosas y Parasitarias, Centro Médico Nacional Siglo XXI-IMSSMexico City, Mexico; Emerging Pathogens Institute, University of FloridaGainesville, FL, USA.
Jason K MorganDepartment of Cell Biology, Microbiology, and Molecular Biology, University of South Florida Tampa, FL, USA.
Miguel A AresUnidad de Investigación Médica en Enfermedades Infecciosas y Parasitarias, Centro Médico Nacional Siglo XXI-IMSS Mexico City, Mexico.
Jorge A Yáñez-SantosFacultad de Estomatología, Benemerita Universidad Autonoma de Puebla Puebla, Mexico.
James T RiordanDepartment of Cell Biology, Microbiology, and Molecular Biology, University of South Florida Tampa, FL, USA.
Jorge A GirónEmerging Pathogens Institute, University of FloridaGainesville, FL, USA; Centro de Deteccion Biomolecular, Benemerita Universidad Autonoma de PueblaPuebla, Mexico.
Benemérita Universidad Autónoma de Puebla · MXCentro Medico Nacional Siglo XXI · MXUniversity of South Florida · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Enterohemorrhagic Escherichia coli (EHEC) is a significant cause of serious human gastrointestinal disease worldwide. EHEC strains contain a pathogenicity island called the locus of enterocyte effacement (LEE), which encodes virulence factors responsible for damaging the gut mucosa. The Cpx envelope stress response of E. coli is controlled by a two-component system (TCS) consisting of a sensor histidine kinase (CpxA) and a cytoplasmic response regulator (CpxR). In this study, we investigated the role of CpxRA in the expression of LEE-encoded virulence factors of EHEC. We found that a mutation in cpxA significantly affected adherence of EHEC to human epithelial cells. Analysis of this mutant revealed the presence of high levels of CpxR which repressed transcription of grlA and ler, the main positive virulence regulators of the LEE, and influenced negatively the production of the type 3 secretion system-associated EspABD translocator proteins. It is known that CpxR activates rpoH (Sigma factor 32), which in turns activates transcription of the lon protease gene. We found that transcription levels of ler and grlA were significantly increased in the lon and cpxA lon mutants suggesting that lon is involved in down-regulating LEE genes. In addition, the Galleria mellonella model of infection was used to analyze the effect of the loss of the cpx and lon genes in EHEC's ability to kill the larvae. We found that the cpxA mutant was significantly deficient at killing the larvae however, the cpxA lon mutant which overexpresses LEE genes in vitro, was unable to kill the larvae, suggesting that virulence in the G. mellonella model is T3SS independent and that CpxA modulates virulence through a yet unknown EHEC-specific factor. Our data provides new insights and broadens our scope into the complex regulatory network of the LEE in which the CpxA sensor kinase plays an important role in a cascade involving both global and virulence regulators.

Indexed as

Gene Expression Regulation, BacterialAnimalsBacterial ProteinsCell Line, TumorEscherichia coli InfectionsEscherichia coli O157Escherichia coli ProteinsHeat-Shock ProteinsHeLa CellsHumansLarvaMothsPhosphoproteinsProtease LaProtein KinasesSigma FactorBacterial ProteinsCpxA protein, E coliCpxR protein, BacteriaEscherichia coli ProteinsGrlA protein, E coliHeat-Shock Proteinsheat-shock sigma factor 32LEE protein, E coliLer protein, E coliLon protein, E coliPhosphoproteinsProtease LaProtein KinasesSigma FactorTrans-ActivatorsType III Secretion SystemsVirulence FactorsCpxRAEHECLEELon proteasesigma factor 32

Identifiers

PMID26904510
PMCPMC4742615
OpenAlexW2285690440

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.