Evidence map›Paper›PMID 17220220›Full record

ArticleJournal of bacteriology2007

A novel two-component signaling system that activates transcription of an enterohemorrhagic Escherichia coli effector involved in remodeling of host actin.

Nicola C Reading, Alfredo G Torres, Melissa M Kendall, David T Hughes, Kaneyoshi Yamamoto, Vanessa Sperandio

Open access · greenAbstract read
In one paragraph

Article in Journal of bacteriology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
7.7field-weighted citation impact, top 2% 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

74 citing papers in PubMed, 133 citations in OpenAlex.

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  15. AIMS microbiology · 2021
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  20. Review

14 more citing papers are in PubMed but not listed here.

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

6 authors at 3 institutions in 2 countries.

Nicola C ReadingDept. of Microbiology, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390-9048, USA.
Alfredo G Torres
Melissa M Kendall
David T Hughes
Kaneyoshi Yamamoto
Vanessa Sperandio
The University of Texas Southwestern Medical Center · USKindai University · JPThe University of Texas Medical Branch at Galveston · US

Funding

Quorum sensing regulation of EHEC virulence genesR01AI053067 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI SPERANDIO, VANESSA · 2003 to 2017
$6.3M
Quorum Sensing Regulation of EHEC Virulence GenesR37AI053067 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI VANESSA SPERANDIO · 2018 to 2026
$5.3M
NIAID NIH HHS AI053067NIAID NIH HHS R01 AI053067NIAID NIH HHS R37 AI053067
6 · The paper itself

Abstract

Enterohemorrhagic Escherichia coli (EHEC) O157:H7 is responsible for worldwide outbreaks of bloody diarrhea, hemorrhagic colitis, and life-threatening hemolytic uremic syndrome. After colonizing the large intestine, EHEC forms attaching and effacing (AE) lesions on intestinal epithelial cells. These lesions cause destruction of the microvilli and elicit actin rearrangement to form pedestals that cup each bacterium individually. EHEC responds to a signal produced by the intestinal microbial flora, autoinducer-3 (AI-3), and the host hormones epinephrine and norepinephrine to activate transcription of the genes involved in AE lesion formation. These three signals, involved in interkingdom communication, are sensed by bacterial sensor kinases. Here we describe a novel two-component system, QseEF (quorum-sensing E. coli regulators E and F), which is part of the AI-3/epinephrine/norepinephrine signaling system. QseE is the sensor kinase and QseF the response regulator. The qseEF genes are cotranscribed, and transcription of qseEF is activated by epinephrine through the QseC sensor. A qseF mutant does not form AE lesions. QseF activates transcription of the gene encoding EspFu, an effector protein translocated to the host cell by the EHEC, which mimics a eukaryotic SH2/SH3 adapter protein to engender actin polymerization during pedestal formation. Expression of the espFu gene from a plasmid restored AE lesion formation to the qseF mutant, suggesting that lack of espFu expression in this mutant was responsible for the loss of pedestal formation. These findings suggest the QseEF is a two-component system involved in the regulation of AE lesion formation by EHEC.

Indexed as

Gene Expression Regulation, BacterialQuorum SensingSignal TransductionActinsCarrier ProteinsEscherichia coli O157Escherichia coli ProteinsHeLa CellsHumansIntracellular Signaling Peptides and ProteinsMutationVirulenceActinsCarrier ProteinsEscherichia coli ProteinsEspFU protein, E coliIntracellular Signaling Peptides and Proteins

Identifiers

PMID17220220
PMCPMC1899401
OpenAlexW2108092779

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.