ArticleNucleic acids research2023
HPr prevents FruR-mediated facilitation of RNA polymerase binding to the fru promoter in Vibrio cholerae.
Article in Nucleic acids research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 2 citations in OpenAlex.
- OmpW-mediated sensing of MUC2 GalNAc contributes to the ileal tropism of Salmonella Typhi.Cell reports · 2026Article
- CRP-dependent DNA anchoring and membrane sequestration define a dual mechanism for MtlR-mediated regulation.Nucleic acids research · 2026Article
- Rapid growth phenotype of carbapenem-resistant Enterobacter cloacae: growth fitness, stability, and mechanistic insights.BMC genomics · 2026Article
- Ag-CuO Nanozymes Superior to Commercial Silver-Based Dressings: Synergistic Antibacterial Therapy via PTS-Mediated Starvation and Cuproptosis-Like Death.Research (Washington, D.C.) · 2026Article
- Fructose-responsive regulation by FruR in Faecalibacterium prausnitzii for its intestinal colonization.Communications biology · 2025Article
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6 authors at 2 institutions in 1 country.
Funding
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Abstract
Phosphorylation state-dependent interactions of the phosphoenolpyruvate (PEP):carbohydrate phosphotransferase system (PTS) components with transcription factors play a key role in carbon catabolite repression (CCR) by glucose in bacteria. Glucose inhibits the PTS-dependent transport of fructose and is preferred over fructose in Vibrio cholerae, but the mechanism is unknown. We have recently shown that, contrary to Escherichia coli, the fructose-dependent transcriptional regulator FruR acts as an activator of the fru operon in V. cholerae and binding of the FruR-fructose 1-phosphate (F1P) complex to an operator facilitates RNA polymerase (RNAP) binding to the fru promoter. Here we show that, in the presence of glucose, dephosphorylated HPr, a general PTS component, binds to FruR. Whereas HPr does not affect DNA-binding affinity of FruR, regardless of the presence of F1P, it prevents the FruR-F1P complex from facilitating the binding of RNAP to the fru promoter. Structural and biochemical analyses of the FruR-HPr complex identify key residues responsible for the V. cholerae-specific FruR-HPr interaction not observed in E. coli. Finally, we reveal how the dephosphorylated HPr interacts with FruR in V. cholerae, whereas the phosphorylated HPr binds to CcpA, which is a global regulator of CCR in Bacillus subtilis and shows structural similarity to FruR.
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