Evidence map›Paper›PMID 38172623›Full record

ArticleNature microbiology2024

The Vibrio cholerae CBASS phage defence system modulates resistance and killing by antifolate antibiotics.

Susanne Brenzinger, Martina Airoldi, Adewale Joseph Ogunleye, Karl Jugovic, Martin Krähenbühl Amstalden, Ana Rita Brochado

Abstract read
PubMed Publisher
In one paragraph

Article in Nature microbiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
12.3field-weighted citation impact, top 1% of its field
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

16 citing papers in PubMed, 22 citations in OpenAlex.

  1. How bacterial immune systems sense phage infection.Nature reviews. Microbiology · 2026
    Review
  2. Members of theMicrobial genomics · 2026
    Article
  3. Article
  4. Review
  5. DNA-intercalating antiphage molecules trigger abortive infection through mutual destruction and synergize with bacterial immunity.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  6. Review
  7. Article
  8. Article
  9. Defence systems encoded by core genomic islands of seventh pandemicPhilosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Activation of amBio · 2023
    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 at 1 institution in 1 country.

Susanne BrenzingerDepartment of Microbiology, Biocenter, University of Würzburg, Würzburg, Germany.ORCID 0000-0003-2854-1194
Martina Airoldi *Department of Microbiology, Biocenter, University of Würzburg, Würzburg, Germany.
Adewale Joseph Ogunleye *Department of Microbiology, Biocenter, University of Würzburg, Würzburg, Germany.
Karl JugovicDepartment of Microbiology, Biocenter, University of Würzburg, Würzburg, Germany.
Martin Krähenbühl AmstaldenDepartment of Microbiology, Biocenter, University of Würzburg, Würzburg, Germany.
Ana Rita BrochadoDepartment of Microbiology, Biocenter, University of Würzburg, Würzburg, Germany. ana.brochado@uni-tuebingen.de.ORCID 0000-0003-1703-383X
University of Würzburg · DE

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) 390838134Deutsche Forschungsgemeinschaft (German Research Foundation) GO 3161/1-1Hector Fellow Academy HRCDA2020 to ARB
6 · The paper itself

Abstract

Toxic bacterial modules such as toxin-antitoxin systems hold antimicrobial potential, though successful applications are rare. Here we show that in Vibrio cholerae the cyclic-oligonucleotide-based anti-phage signalling system (CBASS), another example of a toxic module, increases sensitivity to antifolate antibiotics up to 10×, interferes with their synergy and ultimately enables bacterial lysis by these otherwise classic bacteriostatic antibiotics. Cyclic-oligonucleotide production by the CBASS nucleotidyltransferase DncV upon antifolate treatment confirms full CBASS activation under these conditions, and suggests that antifolates release DncV allosteric inhibition by folates. Consequently, the CBASS-antifolate interaction is specific to CBASS systems with closely related nucleotidyltransferases and similar folate-binding pockets. Last, antifolate resistance genes abolish the CBASS-antifolate interaction by bypassing the effects of on-target antifolate activity, thereby creating potential for their coevolution with CBASS. Altogether, our findings illustrate how toxic modules can impact antibiotic activity and ultimately confer bactericidal activity to classical bacteriostatic antibiotics.

Indexed as

BacteriophagesFolic Acid AntagonistsVibrio choleraeAnti-Bacterial AgentsBacteriaOligonucleotidesAnti-Bacterial AgentsFolic Acid AntagonistsOligonucleotides

Identifiers

PMID38172623
OpenAlexW4390571582

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.