ArticleInfection and immunity2007
QseA directly activates transcription of LEE1 in enterohemorrhagic Escherichia coli.
Article in Infection and immunity, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 66 citations in OpenAlex.
- Intestinal motility shapes spatiotemporal patterns of enterohemorrhagicInfection and immunity · 2026Article
- The small regulatory RNA DsrA silences the locus of enterocyte effacement of enteropathogenicmicroPublication biology · 2025Article
- A master regulator of central carbon metabolism directly activates virulence gene expression in attaching and effacing pathogens.PLoS pathogens · 2024Article
- Enterococcus faecalis-derived adenine enhances enterohaemorrhagic Escherichia coli Type 3 Secretion System-dependent virulence.Nature microbiology · 2024Article
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- Lactobacilli, a Weapon to Counteract Pathogens through the Inhibition of Their Virulence Factors.Journal of bacteriology · 2022Review
- Magnesium Sensing Regulates Intestinal Colonization of Enterohemorrhagic Escherichia coli O157:H7.mBio · 2020Article
- Regulation of the Locus of Enterocyte Effacement in Attaching and Effacing Pathogens.Journal of bacteriology · 2018Review
- Sulfamethoxazole - Trimethoprim represses csgD but maintains virulence genes at 30°C in a clinical Escherichia coli O157:H7 isolate.PloS one · 2018Article
- Environment Controls LEE Regulation in EnteropathogenicFrontiers in microbiology · 2018Review
- Strategies for Biofilm Inhibition and Virulence Attenuation of Foodborne Pathogen-Escherichia coli O157:H7.Current microbiology · 2017Review
- Regulation ofEcoSal Plus · 2017Review
- Hfq and three Hfq-dependent small regulatory RNAs-MgrR, RyhB and McaS-coregulate the locus of enterocyte effacement in enteropathogenic Escherichia coli.Pathogens and disease · 2017Article
- The Type Three Secretion System 2-Encoded Regulator EtrB Modulates Enterohemorrhagic Escherichia coli Virulence Gene Expression.Infection and immunity · 2016Article
- Global Regulator of Virulence A (GrvA) Coordinates Expression of Discrete Pathogenic Mechanisms in Enterohemorrhagic Escherichia coli through Interactions with GadW-GadE.Journal of bacteriology · 2016Article
- A Highly Conserved Bacterial D-Serine Uptake System Links Host Metabolism and Virulence.PLoS pathogens · 2016Article
- Control of acid resistance pathways of enterohemorrhagic Escherichia coli strain EDL933 by PsrB, a prophage-encoded AraC-like regulator.Infection and immunity · 2015Article
- From ingestion to colonization: the influence of the host environment on regulation of the LEE encoded type III secretion system in enterohaemorrhagic Escherichia coli.Frontiers in microbiology · 2015Review
- Escherichia coli O157:H7 lacking the qseBC-encoded quorum-sensing system outcompetes the parental strain in colonization of cattle intestines.Applied and environmental microbiology · 2014Article
- EutR is a direct regulator of genes that contribute to metabolism and virulence in enterohemorrhagic Escherichia coli O157:H7.Journal of bacteriology · 2013Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Quorum sensing (QS) in enterohemorrhagic Escherichia coli (EHEC) regulates the expression of the locus of enterocyte effacement (LEE). The LEE contains five major operons named LEE1 through LEE5. QseA was previously shown to be activated through QS and to activate the transcription of LEE1. The LEE1 operon encodes Ler, the transcription activator of all other LEE genes, and has two promoters: a distal promoter (P1) and a proximal promoter (P2). We have previously reported that QseA acts on P1 and not P2. To identify the minimal region of LEE1 that is necessary for QseA-mediated activation, a series of nested-deletion constructs of the LEE1 promoter fused to a lacZ reporter were constructed in both the EHEC and E. coli K-12 backgrounds. In an EHEC background, QseA-dependent activation of LEE1 can be observed for the entire regulatory region (beginning at nucleotide -393 and ending at nucleotide -123). In contrast to what occurred in EHEC, in K-12 there was no QseA-dependent activation of LEE1 transcription between base pairs -393 and -343. These data indicate that a QseA-dependent EHEC-specific regulator is required for the activation of transcription in this region. We also observed QseA-dependent LEE1 activation from nucleotides -218 to -123 in K-12, similar to results of the nested-deletion analysis performed with EHEC. Electrophoretic mobility shift assays established that QseA directly binds to the region of LEE1 from bp -173 to -42 and not to the region from bp -393 to -343. These studies suggest that QseA activates the transcription of LEE1 by directly binding upstream of its P1 promoter region.
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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.