ArticleJournal of bacteriology2011
Hfq virulence regulation in enterohemorrhagic Escherichia coli O157:H7 strain 86-24.
Article in Journal of bacteriology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 78 citations in OpenAlex.
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- Genomewide transcriptional response of Escherichia coli O157:H7 to norepinephrine.BMC genomics · 2022Article
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- Stepwise sRNA targeting of structured bacterial mRNAs leads to abortive annealing.Molecular cell · 2021Article
- Impacts of Small RNAs and Their Chaperones on Bacterial Pathogenicity.Frontiers in cellular and infection microbiology · 2021Review
- The Serotonin Neurotransmitter Modulates Virulence of Enteric Pathogens.Cell host & microbe · 2020Article
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- Small RNA Regulation of Virulence in PathogenicFrontiers in cellular and infection microbiology · 2020Review
- Enhancement of immune response against Bordetella spp. by disrupting immunomodulation.Scientific reports · 2019Article
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- The sRNA DicF integrates oxygen sensing to enhance enterohemorrhagicProceedings of the National Academy of Sciences of the United States of America · 2019Article
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- Integrated Signaling Pathways Mediate Bordetella Immunomodulation, Persistence, and Transmission.Trends in microbiology · 2019Review
- Epigallocatechin Gallate Remodelling of Hfq Amyloid-Like Region AffectsPathogens (Basel, Switzerland) · 2018Article
- After the Fact(or): Posttranscriptional Gene Regulation in Enterohemorrhagic Escherichia coli O157:H7.Journal of bacteriology · 2018Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Enterohemorrhagic Escherichia coli O157:H7 (EHEC) causes bloody diarrhea and hemolytic-uremic syndrome. EHEC encodes the sRNA chaperone Hfq, which is important in posttranscriptional regulation. In EHEC strain EDL933, Hfq acts as a negative regulator of the locus of enterocyte effacement (LEE), which encodes most of the proteins involved in type III secretion and attaching and effacing (AE) lesions. Here, we deleted hfq in the EHEC strain 86-24 and compared global transcription profiles of the hfq mutant and wild-type (WT) strains in exponential growth phase. Deletion of hfq affected transcription of genes common to nonpathogenic and pathogenic strains of E. coli as well as pathogen-specific genes. Downregulated genes in the hfq mutant included ler, the transcriptional activator of all the LEE genes, as well as genes encoded in the LEE2 to -5 operons. Decreased expression of the LEE genes in the hfq mutant occurred at middle, late, and stationary growth phases. We also confirmed decreased regulation of the LEE genes by examining the proteins secreted and AE lesion formation by the hfq mutant and WT strains. Deletion of hfq also caused decreased expression of the two-component system qseBC, which is involved in interkingdom signaling and virulence gene regulation in EHEC, as well as an increase in expression of stx(2AB), which encodes the deadly Shiga toxin. Altogether, these data indicate that Hfq plays a regulatory role in EHEC 86-24 that is different from what has been reported for EHEC strain EDL933 and that the role of Hfq in EHEC virulence regulation extends beyond the LEE.
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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.