Evidence map›Paper›PMID 39252550›Full record

ArticleJournal of extracellular vesicles2024

The activity of the quorum sensing regulator HapR is modulated by the bacterial extracellular vesicle (BEV)-associated protein ObfA of Vibrio cholerae.

Stephan P Ebenberger, Fatih Cakar, Yi-Chi Chen, Katharina Pressler, Leo Eberl, Stefan Schild

Abstract read
In one paragraph

Article in Journal of extracellular vesicles, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Outer membrane vesicles inMicrobial cell (Graz, Austria) · 2026
    Article
  6. Review
  7. Review
  8. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Stephan P EbenbergerInstitute of Molecular Biosciences, University of Graz, Graz, Austria.ORCID 0009-0005-5843-3831
Fatih CakarInstitute of Molecular Biosciences, University of Graz, Graz, Austria.
Yi-Chi ChenDepartment of Plant and Microbial Biology, University of Zurich, Zurich, Switzerland.ORCID 0000-0003-3819-4085
Katharina PresslerInstitute of Molecular Biosciences, University of Graz, Graz, Austria.
Leo EberlDepartment of Plant and Microbial Biology, University of Zurich, Zurich, Switzerland.
Stefan SchildInstitute of Molecular Biosciences, University of Graz, Graz, Austria.ORCID 0000-0001-7842-0177

Funding

Austrian Science Fund P32577Karl-Franzens-Universität Graz
6 · The paper itself

Abstract

Vibrio cholerae, a facultative human pathogen and causative agent of the severe diarrheal disease cholera, transits between the human intestinal tract and aquatic reservoirs. Like other bacterial species, V. cholerae continuously releases bacterial extracellular vesicles (BEVs) from its surface, which have been recently characterised for their role during in vivo colonisation. However, between epidemic outbreaks, V. cholerae persists in the biofilm mode for extended periods in aquatic reservoirs, which enhances environmental fitness and host transition. In this study, we investigated the effect of V. cholerae BEVs on biofilm formation, a critical feature for ex vivo survival. In contrast to BEVs from planktonic cultures, our results show that physiological concentrations of BEVs from dynamic biofilm cultures facilitate V. cholerae biofilm formation, which could be linked to a proteinaceous factor. Comparative proteomic analyses of planktonic- and biofilm-derived BEVs identified a previously uncharacterised outer membrane protein as an abundant component of dynamic biofilm-derived BEVs, which was found to be responsible for the BEV-dependent enhancement of biofilm production. Consequently, this protein was named outer membrane-associated biofilm facilitating protein A (ObfA). Comprehensive molecular studies unravelled ObfA as a negative modulator of HapR activity. HapR is a key transcriptional regulator of the V. cholerae quorum sensing (QS) cascade acting as a potent repressor of biofilm formation and virulence. Consistently, obfA mutants not only exhibited reduced biofilm production but also reduced colonisation fitness. Surprisingly, our results demonstrate that ObfA does not affect HapR through the canonical QS system but via the Csr-cascade altering the expression of the small regulatory RNAs CsrC and CsrD. In summary, this study elucidates a novel intraspecies BEV-based communication in V. cholerae that influences biofilm formation and colonisation fitness via a new regulatory pathway involving HapR, Csr-cascade and the BEV-associated protein ObfA.

Indexed as

Bacterial ProteinsBiofilmsExtracellular VesiclesQuorum SensingVibrio choleraeBacterial Outer Membrane ProteinsCholeraGene Expression Regulation, BacterialHumansProteomicsBacterial Outer Membrane ProteinsBacterial Proteinsbacterial membrane vesiclesbiofilmCsrAHapRVC1154virulenceVPS

Identifiers

PMID39252550
PMCPMC11386269

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Registered trials

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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.