ArticleBMC microbiology2012
SspA up-regulates gene expression of the LEE pathogenicity island by decreasing H-NS levels in enterohemorrhagic Escherichia coli.
Article in BMC microbiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 34 citations in OpenAlex.
- SspA is a transcriptional regulator of CRISPR adaptation in E. coli.Nucleic acids research · 2025Article
- The DNA damage response ofProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Adaptive evolution of plasmid and chromosome contributes to the fitness of a blaNDM-bearing cointegrate plasmid in Escherichia coli.The ISME journal · 2024Article
- Degradation of gene silencer is essential for expression of foreign genes and bacterial colonization of the mammalian gut.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Parallel Evolution towards Increased Motility in Long-Term Cultures of Escherichia coli, Even Though Motility was Not Required for Long-Term Survival.Microbiology spectrum · 2022Article
- DnaA and SspA regulation of the iraD gene of Escherichia coli: an alternative DNA damage response independent of LexA/RecA.Genetics · 2022Article
- Collective behavior and virulence arsenal of the fish pathogenFrontiers in cellular and infection microbiology · 2022Article
- Stringent Starvation Protein Regulates Prodiginine Biosynthesis via Affecting Siderophore Production inApplied and environmental microbiology · 2021Article
- Article
- Control ofMicroorganisms · 2020Review
- Structural basis for transcription inhibition by E. coli SspA.Nucleic acids research · 2020Article
- Biofilm Bacteria Use Stress Responses to Detect and Respond to Competitors.Current biology : CB · 2020Article
- Chemical Genomics, Structure Elucidation, and in Vivo Studies of the Marine-Derived Anticlostridial Ecteinamycin.ACS chemical biology · 2017Article
- Identification and Characterization of a Bacterial Homolog of Chloride Intracellular Channel (CLIC) Protein.Scientific reports · 2017Article
- Dissection of the molecular circuitry controlling virulence inGenes & development · 2017Article
- Ubiquitous promoter-localization of essential virulence regulators in Francisella tularensis.PLoS pathogens · 2015Article
- Structural and Biochemical Characterization of the Francisella tularensis Pathogenicity Regulator, Macrophage Locus Protein A (MglA).PloS one · 2015Article
- Recent advances in adherence and invasion of pathogenic Escherichia coli.Current opinion in infectious diseases · 2014Review
- Coordinate control of virulence gene expression in Francisella tularensis involves direct interaction between key regulators.Journal of bacteriology · 2014Article
- H-NST induces LEE expression and the formation of attaching and effacing lesions in enterohemorrhagic Escherichia coli.PloS one · 2014Article
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundEnterohemorrhagic Escherichia coli (EHEC) colonizes the intestinal epithelium and causes attaching and effacing (A/E) lesions. Expression of virulence genes, particularly those from the locus of the enterocyte effacement (LEE) pathogenicity island is required for the formation of a type three secretion system, which induces A/E lesion formation. Like other horizontally acquired genetic elements, expression of the LEE is negatively regulated by H-NS. In the non-pathogenic Escherichia coli K-12 strain the stringent starvation protein A (SspA) inhibits accumulation of H-NS, and thereby allows de-repression of the H-NS regulon during the stationary phase of growth. However, the effect of SspA on the expression of H-NS-controlled virulence genes in EHEC is unknown.
resultsHere we assess the effect of SspA on virulence gene expression in EHEC. We show that transcription of virulence genes including those of the LEE is decreased in an sspA mutant, rendering the mutant strain defective in forming A/E lesions. A surface exposed pocket of SspA is functionally important for the regulation of the LEE and for the A/E phenotype. Increased expression of ler alleviates LEE expression in an sspA mutant, suggesting that the level of Ler in the mutant is insufficient to counteract H-NS-mediated repression. We demonstrate that the H-NS level is two-fold higher in an sspA mutant compared to wild type, and that the defects of the sspA mutant are suppressed by an hns null mutation, indicating that hns is epistatic to sspA in regulating H-NS repressed virulence genes.
conclusionsSspA positively regulates the expression of EHEC virulence factors by restricting the intracellular level of H-NS. Since SspA is conserved in many bacterial pathogens containing horizontally acquired pathogenicity islands controlled by H-NS, our study suggests a common mechanism whereby SspA potentially regulates the expression of virulence genes in these pathogens.
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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.