Evidence map›Paper›PMID 37683045›Full record

ArticlePLoS pathogens2023

Replication cycle timing determines phage sensitivity to a cytidine deaminase toxin/antitoxin bacterial defense system.

Brian Y Hsueh, Micah J Ferrell, Ram Sanath-Kumar, Amber M Bedore, Christopher M Waters

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

11 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Defence systems encoded by core genomic islands of seventh pandemicPhilosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. AJournal of bacteriology · 2024
    Article
  11. AbioRxiv : the preprint server for biology · 2024
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Brian Y HsuehDepartment of Microbiology and Molecular Genetics, Michigan State University, East Lansing, Michigan, United States of America.
Micah J FerrellDepartment of Microbiology and Molecular Genetics, Michigan State University, East Lansing, Michigan, United States of America.
Ram Sanath-KumarDepartment of Microbiology and Molecular Genetics, Michigan State University, East Lansing, Michigan, United States of America.
Amber M BedoreDepartment of Microbiology and Molecular Genetics, Michigan State University, East Lansing, Michigan, United States of America.
Christopher M WatersDepartment of Microbiology and Molecular Genetics, Michigan State University, East Lansing, Michigan, United States of America.ORCID 0000-0003-2336-7836
Michigan United · US

Funding

Gender, Migration, and HIV Risks Among MexicansR01NR008052 · NINR · UNIVERSITY OF PENNSYLVANIA · PI PARRADO, EMILIO ALBERTO · 2001 to 2008
$3.4M
Exploring cyclic di-nucleotide signaling across the tree of life (Supplement)R35GM139537 · NIGMS · MICHIGAN STATE UNIVERSITY · PI WATERS, CHRISTOPHER M · 2021 to 2025
$2.9M
The contribution of novel cytidine deaminase regulatory systems to bacterial evolutionR01AI158433 · NIAID · MICHIGAN STATE UNIVERSITY · PI NEIDITCH, MATTHEW B, WATERS, CHRISTOPHER M · 2021 to 2025
$2.9M
NIAID NIH HHS R01 AI158433NIGMS NIH HHS R35 GM139537NINR NIH HHS R01 NR008052
6 · The paper itself

Abstract

Toxin-antitoxin (TA) systems are ubiquitous two-gene loci that bacteria use to regulate cellular processes such as phage defense. Here, we demonstrate the mechanism by which a novel type III TA system, avcID, is activated and confers resistance to phage infection. The toxin of the system (AvcD) is a deoxycytidylate deaminase that converts deoxycytidines (dC) to dexoyuridines (dU), while the RNA antitoxin (AvcI) inhibits AvcD activity. We have shown that AvcD deaminated dC nucleotides upon phage infection, but the molecular mechanism that activated AvcD was unknown. Here we show that the activation of AvcD arises from phage-induced inhibition of host transcription, leading to degradation of the labile AvcI. AvcD activation and nucleotide depletion not only decreases phage replication but also increases the formation of defective phage virions. Surprisingly, infection of phages such as T7 that are not inhibited by AvcID also lead to AvcI RNA antitoxin degradation and AvcD activation, suggesting that depletion of AvcI is not sufficient to confer protection against some phage. Rather, our results support that phage with a longer replication cycle like T5 are sensitive to AvcID-mediated protection while those with a shorter replication cycle like T7 are resistant.

Indexed as

AntitoxinsBacteriophagesBacteriaCytidine DeaminaseNucleotidesRNAAntitoxinsCytidine DeaminaseNucleotidesRNA

Identifiers

PMID37683045
PMCPMC10511110
OpenAlexW4386534186

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.