ArticleMolecular microbiology2018
Insights into transcriptional silencing and anti-silencing in Shigella flexneri: a detailed molecular analysis of the icsP virulence locus.
Article in Molecular microbiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- Contrasting regulation of the ecp common pilus operon in Citrobacter rodentium: essential roles of a distal element and IHF even in the absence of H-NS.Archives of microbiology · 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
- Remote Regulation by VirB, the Transcriptional Anti-Silencer of Shigella Virulence Genes, Provides Mechanistic Information.Molecular microbiology · 2025Article
- The virulence regulator VirB from Shigella flexneri uses a CTP-dependent switch mechanism to activate gene expression.Nature communications · 2024Article
- VirB, a transcriptional activator of virulence in Shigella flexneri, uses CTP as a cofactor.Communications biology · 2023Article
- VirB, a key transcriptional regulator ofmBio · 2023Article
- A Tale aboutMicroorganisms · 2023Review
- VirB, a key transcriptional regulator ofbioRxiv : the preprint server for biology · 2023Article
- Localized modulation of DNA supercoiling, triggered by the Shigella anti-silencer VirB, is sufficient to relieve H-NS-mediated silencing.Nucleic acids research · 2023Article
- Article
- The AraC/XylS Protein MxiE and Its Coregulator IpgC Control a Negative Feedback Loop in the Transcriptional Cascade That Regulates Type III Secretion in Shigella flexneri.Journal of bacteriology · 2022Article
- VirB, a key transcriptional regulator of virulence plasmid genes inJournal of bacteriology · 2021Article
- The T3SS ofMicroorganisms · 2020Review
- The Antiactivator of Type III Secretion, OspD1, Is Transcriptionally Regulated by VirB and H-NS from Remote Sequences in Shigella flexneri.Journal of bacteriology · 2020Article
- Maintenance of the virulence plasmid in Shigella flexneri is influenced by Lon and two functional partitioning systems.Molecular microbiology · 2019Article
- Article
- Regulatory Hierarchies Controlling Virulence Gene Expression inFrontiers in microbiology · 2018Review
Corrections and comments
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Authors and funding
17 authors at 1 institution in 1 country.
Funding
Abstract
Transcriptional silencing and anti-silencing mechanisms modulate bacterial physiology and virulence in many human pathogens. In Shigella species, many virulence plasmid genes are silenced by the histone-like nucleoid structuring protein H-NS and anti-silenced by the virulence gene regulator VirB. Despite the key role that these regulatory proteins play in Shigella virulence, their mechanisms of transcriptional control remain poorly understood. Here, we characterize the regulatory elements and their relative spacing requirements needed for the transcriptional silencing and anti-silencing of icsP, a locus that requires remotely located regulatory elements for both types of transcriptional control. Our findings highlight the flexibility of the regulatory elements' positions with respect to each other, and yet, a molecular roadblock docked between the VirB binding site and the upstream H-NS binding region abolishes transcriptional anti-silencing by VirB, providing insight into transcriptional anti-silencing. Our study also raises the need to re-evaluate the currently proposed VirB binding site. Models of transcriptional silencing and anti-silencing at this genetic locus are presented, and the implications for understanding these regulatory mechanisms in bacteria are discussed.
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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.