ArticlePloS one2014
H-NST induces LEE expression and the formation of attaching and effacing lesions in enterohemorrhagic Escherichia coli.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- Post-translational modifications of the nucleoid protein H-NS: sites, mechanisms, and regulatory cues.FEMS microbiology reviews · 2025Review
- The RNA-binding protein ProQ directly binds and regulates virulence genes in enterohemorrhagicFrontiers in cellular and infection microbiology · 2025Article
- Bacterial chromatin proteins, transcription, and DNA topology: Inseparable partners in the control of gene expression.Molecular microbiology · 2024Review
- Advancing evolution: Bacteria break down gene silencer to express horizontally acquired genes.BioEssays : news and reviews in molecular, cellular and developmental biology · 2023Article
- Xenogeneic nucleoid-associated EnrR thwarts H-NS silencing of bacterial virulence with unique DNA binding.Nucleic acids research · 2022Article
- Review
- Impact of Xenogeneic Silencing on Phage-Host Interactions.Journal of molecular biology · 2019Review
- Transcription of Bacterial Chromatin.Journal of molecular biology · 2019Review
- Endogenous and Foreign Nucleoid-Associated Proteins of Bacteria: Occurrence, Interactions and Effects on Mobile Genetic Elements and Host's Biology.Computational and structural biotechnology journal · 2019Review
- Article
- Type Three Secretion System in Attaching and Effacing Pathogens.Frontiers in cellular and infection microbiology · 2016Review
- Identification and regulation of a novel Citrobacter rodentium gut colonization fimbria (Gcf).Journal of bacteriology · 2015Article
- Integrated circuits: how transcriptional silencing and counter-silencing facilitate bacterial evolution.Current opinion in microbiology · 2015Review
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Authors and funding
6 authors.
Funding
Abstract
backgroundEnteropathogenic E. coli (EPEC) and enterohemorrhagic E. coli are important causes of morbidity and mortality worldwide. These enteric pathogens contain a type III secretion system (T3SS) responsible for the attaching and effacing (A/E) lesion phenotype. The T3SS is encoded by the locus of enterocyte effacement (LEE) pathogenicity island. The H-NS-mediated repression of LEE expression is counteracted by Ler, the major activator of virulence gene expression in A/E pathogens. A regulator present in EPEC, H-NST, positively affects expression of H-NS regulon members in E. coli K-12, although the effect of H-NST on LEE expression and virulence of A/E pathogens has yet-to-be determined.
resultsWe examine the effect of H-NST on LEE expression and A/E lesion formation on intestinal epithelial cells. We find that H-NST positively affects the levels of LEE-encoded proteins independently of ler and induces A/E lesion formation. We demonstrate H-NST binding to regulatory regions of LEE1 and LEE3, the first report of DNA-binding by H-NST. We characterize H-NST mutants substituted at conserved residues including Ala16 and residues Arg60 and Arg63, which are part of a potential DNA-binding domain. The single mutants A16V, A16L, R60Q and the double mutant R60Q/R63Q exhibit a decreased effect on LEE expression and A/E lesion formation. DNA mobility shift assays reveal that these residues are important for H-NST to bind regulatory LEE DNA targets. H-NST positively affects Ler binding to LEE DNA in the presence of H-NS, and thereby potentially helps Ler displace H-NS bound to DNA.
conclusionsH-NST induces LEE expression and A/E lesion formation likely by counteracting H-NS-mediated repression. We demonstrate that H-NST binds to DNA and identify arginine residues that are functionally important for DNA-binding. Our study suggests that H-NST provides an additional means for A/E pathogens to alleviate repression of virulence gene expression by H-NS to promote virulence capabilities.
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