ArticleJournal of bacteriology2016
Global Regulator of Virulence A (GrvA) Coordinates Expression of Discrete Pathogenic Mechanisms in Enterohemorrhagic Escherichia coli through Interactions with GadW-GadE.
Article in Journal of bacteriology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 17 citations in OpenAlex.
- Bile-mediated ToxS homodimerization provides a model for ToxRS periplasmic interactions.bioRxiv : the preprint server for biology · 2026Article
- Genomic island-encoded LmiA regulates acid resistance and biofilm formation in enterohemorrhagicGut microbes · 2025Article
- Review
- The type 6 secretion system immunity protein RhsFI has been repurposed for small RNA regulation in pathogenic Escherichia coli.Nucleic acids research · 2025Article
- Genomic island-encoded regulatory proteins in enterohemorrhagicVirulence · 2024Review
- Transmembrane Transcription Regulators Are Widespread in Bacteria and Archaea.Microbiology spectrum · 2023Article
- Co-component signal transduction systems: Fast-evolving virulence regulation cassettes discovered in enteric bacteria.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Regulation ofMicrobiology (Reading, England) · 2022Article
- Effect of diet on pathogen performance in the microbiome.Microbiome research reports · 2022Review
- Control freaks-signals and cues governing the regulation of virulence in attaching and effacing pathogens.Biochemical Society transactions · 2019Review
- Article
- Enterohemorrhagic Escherichia coli outwits hosts through sensing small molecules.Current opinion in microbiology · 2018Review
- Regulation ofEcoSal Plus · 2017Review
- Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
unlabelledGlobal regulator of virulence A (GrvA) is a ToxR-family transcriptional regulator that activates locus of enterocyte effacement (LEE)-dependent adherence in enterohemorrhagic Escherichia coli (EHEC). LEE activation by GrvA requires the Rcs phosphorelay response regulator RcsB and is sensitive to physiologically relevant concentrations of bicarbonate, a known stimulant of virulence systems in intestinal pathogens. This study determines the genomic scale of GrvA-dependent regulation and uncovers details of the molecular mechanism underlying GrvA-dependent regulation of pathogenic mechanisms in EHEC. In a grvA-null background of EHEC strain TW14359, RNA sequencing analysis revealed the altered expression of over 700 genes, including the downregulation of LEE- and non-LEE-encoded effectors and the upregulation of genes for glutamate-dependent acid resistance (GDAR). Upregulation of GDAR genes corresponded with a marked increase in acid resistance. GrvA-dependent regulation of GDAR and the LEE required gadE, the central activator of GDAR genes and a direct repressor of the LEE. Control of gadE by GrvA was further determined to occur through downregulation of the gadE activator GadW. This interaction of GrvA with GadW-GadE represses the acid resistance phenotype, while it concomitantly activates the LEE-dependent adherence and secretion of immune subversion effectors. The results of this study significantly broaden the scope of GrvA-dependent regulation and its role in EHEC pathogenesis. IMPORTANCE: Enterohemorrhagic Escherichia coli (EHEC) is an intestinal human pathogen causing acute hemorrhagic colitis and life-threatening hemolytic-uremic syndrome. For successful transmission and gut colonization, EHEC relies on the glutamate-dependent acid resistance (GDAR) system and a type III secretion apparatus, encoded on the LEE pathogenicity island. This study investigates the mechanism whereby the DNA-binding regulator GrvA coordinates activation of the LEE with repression of GDAR. Investigating how these systems are regulated leads to an understanding of pathogenic behavior and novel strategies aimed at disease prevention and control.
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