Evidence map›Paper›PMID 30905288›Full record

ArticlePhilosophical transactions of the Royal Society of London. Series B, Biological sciences2019

Competition between mobile genetic elements drives optimization of a phage-encoded CRISPR-Cas system: insights from a natural arms race.

Amelia C McKitterick, Kristen N LeGault, Angus Angermeyer, Munirul Alam, Kimberley D Seed

Open access · hybridAbstract read
In one paragraph

Article in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

31 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
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  4. AJournal of bacteriology · 2024
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  7. AbioRxiv : the preprint server for biology · 2024
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  8. March of the proviruses.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  9. AeLife · 2024
    Article
  10. Demographic fluctuations in bloodstreamnpj antimicrobials and resistance · 2024
    Article
  11. AbioRxiv : the preprint server for biology · 2023
    Article
  12. Article
  13. 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
  14. Article
  15. Article
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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

5 authors at 3 institutions in 2 countries.

Amelia C McKitterick1 Department of Plant and Microbial Biology, University of California , 111 Koshland Hall, Berkeley, CA 94720 , USA.
Kristen N LeGault1 Department of Plant and Microbial Biology, University of California , 111 Koshland Hall, Berkeley, CA 94720 , USA.
Angus Angermeyer1 Department of Plant and Microbial Biology, University of California , 111 Koshland Hall, Berkeley, CA 94720 , USA.
Munirul Alam2 International Centre for Diarrhoeal Disease Research , Dhaka , Bangladesh.
Kimberley D Seed1 Department of Plant and Microbial Biology, University of California , 111 Koshland Hall, Berkeley, CA 94720 , USA.
University of California, Berkeley · USChan Zuckerberg Initiative (United States) · USInternational Centre for Diarrhoeal Disease Research · BD

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 AI127652
6 · The paper itself

Abstract

CRISPR-Cas systems function as adaptive immune systems by acquiring nucleotide sequences called spacers that mediate sequence-specific defence against competitors. Uniquely, the phage ICP1 encodes a Type I-F CRISPR-Cas system that is deployed to target and overcome PLE, a mobile genetic element with anti-phage activity in Vibrio cholerae. Here, we exploit the arms race between ICP1 and PLE to examine spacer acquisition and interference under laboratory conditions to reconcile findings from wild populations. Natural ICP1 isolates encode multiple spacers directed against PLE, but we find that single spacers do not interfere equally with PLE mobilization. High-throughput sequencing to assay spacer acquisition reveals that ICP1 can also acquire spacers that target the V. cholerae chromosome. We find that targeting the V. cholerae chromosome proximal to PLE is sufficient to block PLE and is dependent on Cas2-3 helicase activity. We propose a model in which indirect chromosomal spacers are able to circumvent PLE by Cas2-3-mediated processive degradation of the V. cholerae chromosome before PLE mobilization. Generally, laboratory-acquired spacers are much more diverse than the subset of spacers maintained by ICP1 in nature, showing how evolutionary pressures can constrain CRISPR-Cas targeting in ways that are often not appreciated through in vitro analyses. This article is part of a discussion meeting issue 'The ecology and evolution of prokaryotic CRISPR-Cas adaptive immune systems'.

Indexed as

BacteriophagesCRISPR-Cas SystemsHigh-Throughput Nucleotide SequencingInterspersed Repetitive SequencesVibrio choleraecholeraCRISPRmobile genetic elementsphage

Identifiers

PMID30905288
PMCPMC6452262
OpenAlexW2887744546

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.