Evidence map›Paper›PMID 29904071›Full record

ArticleNature communications2018

Anti-phage islands force their target phage to directly mediate island excision and spread.

Amelia C McKitterick, Kimberley D Seed

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
7.6field-weighted citation impact, top 2% 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

45 citing papers in PubMed, 81 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Lineage-specific defence systems of pandemicPhilosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
    Review
  6. Article
  7. Article
  8. Genetics, ecology and evolution of phage satellites.Nature reviews. Microbiology · 2025
    Review
  9. Article
  10. Article
  11. Article
  12. Targeted deletion of Pf prophages from diverseJournal of bacteriology · 2024
    Article
  13. AeLife · 2024
    Article
  14. Sporadic phage defense in epidemicbioRxiv : the preprint server for biology · 2023
    Article
  15. Targeted deletion of Pf prophages from diversebioRxiv : the preprint server for biology · 2023
    Article
  16. Open questions in the social lives of viruses.Journal of evolutionary biology · 2023
    Review
  17. AbioRxiv : the preprint server for biology · 2023
    Article
  18. Article
  19. Mechanistic insights into DNA binding and cleavage by a compact type I-F CRISPR-Cas system in bacteriophage.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  20. 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

2 authors at 2 institutions in 1 country.

Amelia C McKitterickDepartment of Plant and Microbial Biology, University of California, Berkeley, 111 Koshland Hall, Berkeley, CA, 94720, USA.
Kimberley D SeedDepartment of Plant and Microbial Biology, University of California, Berkeley, 111 Koshland Hall, Berkeley, CA, 94720, USA. kseed@berkeley.edu.ORCID http://orcid.org/0000-0002-0139-1600
Chan Zuckerberg Initiative (United States) · USUniversity of California, Berkeley · US

Funding

Phage resistance and mobile genetic elements in Vibrio choleraeR01AI127652 · NIAID · UNIVERSITY OF CALIFORNIA BERKELEY · PI SEED, KIMBERLEY DIANE · 2016 to 2025
$4.6M
NIAID NIH HHS R01 AI127652U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID) R01AI127652
6 · The paper itself

Abstract

Vibrio cholerae, the causative agent of the diarrheal disease cholera, is antagonized by the lytic phage ICP1 in the aquatic environment and in human hosts. Mobile genetic elements called PLEs (phage-inducible chromosomal island-like elements) protect V. cholerae from ICP1 infection and initiate their anti-phage response by excising from the chromosome. Here, we show that PLE 1 encodes a large serine recombinase, Int, that exploits an ICP1-specific protein as a recombination directionality factor (RDF) to excise PLE 1 in response to phage infection. We show that this phage-encoded protein is sufficient to direct Int-mediated recombination in vitro and that it is highly conserved in all sequenced ICP1 genomes. Our results uncover an aspect of the molecular specificity underlying the conflict between a single predatory phage and V. cholerae PLE and contribute to our understanding of long-term evolution between phage and their bacterial hosts.

Indexed as

Interspersed Repetitive SequencesBacteriophagesConserved SequenceCRISPR-Cas SystemsDNA, BacterialGenome, BacterialGenomicsOpen Reading FramesPolymerase Chain ReactionProtein DomainsRecombination, GeneticVibrio choleraeViral ProteinsDNA, BacterialPexA protein, bacteriophage ICP1Viral Proteins

Identifiers

PMID29904071
PMCPMC6002521
OpenAlexW2951702576

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.