Evidence map›Paper›PMID 19325886›Full record

ArticlePLoS genetics2009

A toxin-antitoxin system promotes the maintenance of an integrative conjugative element.

Rachel A F Wozniak, Matthew K Waldor

Abstract read
In one paragraph

Article in PLoS genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers.

0numbers the graph read from it
0cells of the map it votes in
128citing 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

128 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Genomic Insights into Emerging Multidrug-ResistantAntibiotics (Basel, Switzerland) · 2025
    Article
  7. Article
  8. Characterization ofFrontiers in microbiology · 2025
    Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. TheApplied and environmental microbiology · 2024
    Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Review
  20. Article

68 more citing papers are in PubMed but not listed here.

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

2 authors.

Rachel A F WozniakChanning Laboratory, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Matthew K Waldor

Funding

Vibrio cholerae intestinal colonization and vaccine developmentR01AI042347 · NIAID · TUFTS UNIVERSITY BOSTON · PI WALDOR, MATTHEW K · 1998 to 2025
$7.3M
Molecular Biology and Virulence of CTX PhageR37AI042347 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI WALDOR, MATTHEW K · 2008 to 2017
$3.8M
Howard Hughes Medical InstituteNIAID NIH HHS AI-042347NIAID NIH HHS R01 AI042347NIAID NIH HHS R37 AI042347
6 · The paper itself

Abstract

SXT is an integrative and conjugative element (ICE) that confers resistance to multiple antibiotics upon many clinical isolates of Vibrio cholerae. In most cells, this approximately 100 Kb element is integrated into the host genome in a site-specific fashion; however, SXT can excise to form an extrachromosomal circle that is thought to be the substrate for conjugative transfer. Daughter cells lacking SXT can theoretically arise if cell division occurs prior to the element's reintegration. Even though approximately 2% of SXT-bearing cells contain the excised form of the ICE, cells that have lost the element have not been detected. Here, using a positive selection-based system, SXT loss was detected rarely at a frequency of approximately 1 x 10(-7). As expected, excision appears necessary for loss, and factors influencing the frequency of excision altered the frequency of SXT loss. We screened the entire 100 kb SXT genome and identified two genes within SXT, now designated mosA and mosT (for maintenance of SXT Antitoxin and Toxin), that promote SXT stability. These two genes, which lack similarity to any previously characterized genes, encode a novel toxin-antitoxin pair; expression of mosT greatly impaired cell growth and mosA expression ameliorated MosT toxicity. Factors that promote SXT excision upregulate mosAT expression. Thus, when the element is extrachromosomal and vulnerable to loss, SXT activates a TA module to minimize the formation of SXT-free cells.

Indexed as

AntitoxinsBacterial ToxinsDrug Resistance, MicrobialEscherichia coliGenes, BacterialGenome, BacterialVibrio choleraeAntitoxinsBacterial Toxins

Identifiers

PMID19325886
PMCPMC2654960

What OpenQuestion holds

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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.