ArticlePLoS pathogens2014
NsrR, GadE, and GadX interplay in repressing expression of the Escherichia coli O157:H7 LEE pathogenicity island in response to nitric oxide.
Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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.
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.
Who cites it
37 citing papers in PubMed, 54 citations in OpenAlex.
- Comparative Genomic and Phylogenetic Analysis ofTransboundary and emerging diseases · 2025Article
- Nitric oxide sensor NsrR is the key direct regulator of magnetosome formation and nitrogen metabolism in Magnetospirillum.Nucleic acids research · 2024Article
- Regulation ofMicrobiology (Reading, England) · 2022Article
- Genomewide transcriptional response of Escherichia coli O157:H7 to norepinephrine.BMC genomics · 2022Article
- Nitric Oxide InducedMicroorganisms · 2022Article
- Article
- Interplay between enterohaemorrhagicEmerging microbes & infections · 2020Article
- Magnesium Sensing Regulates Intestinal Colonization of Enterohemorrhagic Escherichia coli O157:H7.mBio · 2020Article
- Role of the Nitric Oxide Reductase NorVW in the Survival and Virulence of EnterohaemorrhagicPathogens (Basel, Switzerland) · 2020Article
- The Signaling Molecule Indole Inhibits Induction of the AR2 Acid Resistance System inFrontiers in microbiology · 2020Article
- Identification and prevalence of in vivo-induced genes in enterohaemorrhagic Escherichia coli.Virulence · 2019Article
- Porcine Alveolar Macrophages' Nitric Oxide Synthase-Mediated Generation of Nitric Oxide Exerts Important Defensive Effects againstPathogens (Basel, Switzerland) · 2019Article
- Distinct intraspecies virulence mechanisms regulated by a conserved transcription factor.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Diverse effects of nitric oxide reductase NorV on Aeromonas hydrophila virulence-associated traits under aerobic and anaerobic conditions.Veterinary research · 2019Article
- SGI-4 in MonophasicFrontiers in microbiology · 2019Article
- Modulation of EnterohaemorrhagicMicroorganisms · 2018Review
- Nitric oxide-enhanced Shiga toxin production was regulated by Fur and RecA in enterohemorrhagic Escherichia coli O157.MicrobiologyOpen · 2017Article
- Regulation ofEcoSal Plus · 2017Review
- TheVeterinary and animal science · 2017Article
- Pathogen control at the intestinal mucosa - HGut microbes · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Expression of genes of the locus of enterocyte effacement (LEE) is essential for adherence of enterohemorrhagic Escherichia coli (EHEC) to intestinal epithelial cells. Gut factors that may modulate LEE gene expression may therefore influence the outcome of the infection. Because nitric oxide (NO) is a critical effector of the intestinal immune response that may induce transcriptional regulation in enterobacteria, we investigated its influence on LEE expression in EHEC O157:H7. We demonstrate that NO inhibits the expression of genes belonging to LEE1, LEE4, and LEE5 operons, and that the NO sensor nitrite-sensitive repressor (NsrR) is a positive regulator of these operons by interacting directly with the RNA polymerase complex. In the presence of NO, NsrR detaches from the LEE1/4/5 promoter regions and does not activate transcription. In parallel, two regulators of the acid resistance pathway, GadE and GadX, are induced by NO through an indirect NsrR-dependent mechanism. In this context, we show that the NO-dependent LEE1 down-regulation is due to absence of NsrR-mediated activation and to the repressor effect of GadX. Moreover, the inhibition of expression of LEE4 and LEE5 by NO is due to loss of NsrR-mediated activation, to LEE1 down-regulation and to GadE up-regulation. Lastly, we establish that chemical or cellular sources of NO inhibit the adherence of EHEC to human intestinal epithelial cells. These results highlight the critical effect of NsrR in the regulation of the LEE pathogenicity island and the potential role of NO in the limitation of colonization by EHEC.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.