ArticleJournal of bacteriology2010
The LysR-type transcriptional regulator QseD alters type three secretion in enterohemorrhagic Escherichia coli and motility in K-12 Escherichia coli.
Article in Journal of bacteriology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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.
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Who cites it
19 citing papers in PubMed, 33 citations in OpenAlex.
- Genomic island-encoded regulatory proteins in enterohemorrhagicVirulence · 2024Review
- Novel function of single-target regulator NorR involved in swarming motility and biofilm formation revealed in Vibrio alginolyticus.BMC biology · 2024Article
- Complete Genome Sequence Analysis ofFrontiers in microbiology · 2022Article
- LeuO, a LysR-Type Transcriptional Regulator, Is Involved in Biofilm Formation and Virulence ofFrontiers in cellular and infection microbiology · 2021Article
- The Salmonella enterica Serovar TyphiJournal of bacteriology · 2020Article
- Contributions of a LysR Transcriptional Regulator to Listeria monocytogenes Virulence and Identification of Its Regulons.Journal of bacteriology · 2020Article
- LysR-type transcriptional regulator OvrB encoded in O island 9 drives enterohemorrhagicVirulence · 2019Article
- Article
- A Novel Tetrameric Assembly Configuration in VV2_1132, a LysR-Type Transcriptional Regulator inMolecules and cells · 2018Article
- Regulation of the Locus of Enterocyte Effacement in Attaching and Effacing Pathogens.Journal of bacteriology · 2018Review
- Molecular characterization of locus of enterocyte effacement pathogenicity island in shigatoxicThe Indian journal of medical research · 2017Article
- QseBC, a two-component bacterial adrenergic receptor and global regulator of virulence in Enterobacteriaceae and Pasteurellaceae.Molecular oral microbiology · 2016Review
- 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
- Locus of enterocyte effacement: a pathogenicity island involved in the virulence of enteropathogenic and enterohemorragic Escherichia coli subjected to a complex network of gene regulation.BioMed research international · 2015Review
- A predictor for predicting Escherichia coli transcriptome and the effects of gene perturbations.BMC bioinformatics · 2014Article
- 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
- Identification of a hypochlorite-specific transcription factor from Escherichia coli.The Journal of biological chemistry · 2012Article
- luxS mutant regulation: quorum sensing impairment or methylation disorder?Sensors (Basel, Switzerland) · 2012Article
- Coordinate control of the locus of enterocyte effacement and enterohemolysin genes by multiple common virulence regulators in enterohemorrhagic Escherichia coli.Infection and immunity · 2011Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Enterohemorrhagic Escherichia coli (EHEC) O157:H7 responds to the host-produced epinephrine and norepinephrine, and bacterially produced autoinducer 3 (AI-3), through two-component systems. Further integration of multiple regulatory signaling networks, involving regulators such as the LysR-type transcriptional regulator (LTTR) QseA, promotes effective regulation of virulence factors. These include the production of flagella, a phage-encoded Shiga toxin, and genes within the locus of enterocyte effacement (LEE) responsible for attaching and effacing (AE) lesion formation. Here, we describe a new member of this signaling cascade, an LTTR heretofore renamed QseD (quorum-sensing E. coli regulator D). QseD is present in all enterobacteria but exists almost exclusively in O157:H7 isolates as a helix-turn-helix (HTH) truncated isoform. This "short" isoform (sQseD) is still able to regulate gene expression through a different mechanism than the full-length K-12 E. coli "long" QseD isoform (lQseD). The EHEC Delta qseD mutant exhibits increased expression of all LEE operons and deregulation of AE lesion formation. The loss of qseD in EHEC does not affect motility, but the K-12 Delta qseD mutant is hypermotile. While the lQseD directly binds to the ler promoter, encoding the LEE master regulator, to repress LEE transcription, the sQseD isoform does not. LTTRs bind to DNA as tetramers, and these data suggest that sQseD regulates ler by forming heterotetramers with another LTTR. The LTTRs known to regulate LEE transcription, QseA and LrhA, do not interact with sQseD, suggesting that sQseD acts as a dominant-negative partner with a yet-unidentified LTTR.
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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.