ArticleCommunications biology2023
VirB, a transcriptional activator of virulence in Shigella flexneri, uses CTP as a cofactor.
Article in Communications biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- TrbA binds and locks a sliding clamp KorB to repress transcription on multi-drug resistance plasmids.Journal of bacteriology · 2026Article
- The role of the VirB ligand CTP in the molecular mechanism of transcriptional anti-silencing in Shigella flexneri.Nucleic acids research · 2026Article
- Versatile NTP recognition and domain fusions expand the functional repertoire of the ParB-CTPase fold beyond chromosome segregation.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Orchestrated long-distance gene activation by a ParB-like BisD-CTP DNA clamp in low-frequency transfer competence development in Pseudomonas putida.Nucleic acids research · 2025Article
- Remote Regulation by VirB, the Transcriptional Anti-Silencer of Shigella Virulence Genes, Provides Mechanistic Information.Molecular microbiology · 2025Article
- KorB switching from DNA-sliding clamp to repressor mediates long-range gene silencing in a multi-drug resistance plasmid.Nature microbiology · 2025Article
- Post-translational modifications of the nucleoid protein H-NS: sites, mechanisms, and regulatory cues.FEMS microbiology reviews · 2025Review
- Connecting the dots: key insights on ParB for chromosome segregation from single-molecule studies.FEMS microbiology reviews · 2024Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
VirB is a transcriptional activator of virulence in the gram-negative bacterium Shigella flexneri encoded by the large invasion plasmid, pINV. It counteracts the transcriptional silencing by the nucleoid structuring protein, H-NS. Mutations in virB lead to loss of virulence. Studies suggested that VirB binds to specific DNA sequences, remodels the H-NS nucleoprotein complexes, and changes DNA supercoiling. VirB belongs to the superfamily of ParB proteins which are involved in plasmid and chromosome partitioning often as part of a ParABS system. Like ParB, VirB forms discrete foci in Shigella flexneri cells harbouring pINV. Our results reveal that purified preparations of VirB specifically bind the ribonucleotide CTP and slowly but detectably hydrolyse it with mild stimulation by the virS targeting sequences found on pINV. We show that formation of VirB foci in cells requires a virS site and CTP binding residues in VirB. Curiously, DNA stimulation of clamp closure appears efficient even without a virS sequence in vitro. Specificity for entrapment of virS DNA is however evident at elevated salt concentrations. These findings suggest that VirB acts as a CTP-dependent DNA clamp and indicate that the cellular microenvironment contributes to the accumulation of VirB specifically at virS sites.
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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.