Evidence map›Paper›PMID 24990370›Full record

ArticleNucleic acids research2014

Priming in the Type I-F CRISPR-Cas system triggers strand-independent spacer acquisition, bi-directionally from the primed protospacer.

Corinna Richter, Ron L Dy, Rebecca E McKenzie, Bridget N J Watson, Corinda Taylor, James T Chang, Matthew B McNeil, Raymond H J Staals, Peter C Fineran

Abstract read
In one paragraph

Article in Nucleic acids research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers.

0numbers the graph read from it
0cells of the map it votes in
113citing 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

113 citing papers in PubMed.

  1. Review
  2. Phage susceptibility to a minimal, modular synthetic CRISPR-Cas system inPhilosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
    Article
  3. Review
  4. CRISPR-Cas Systems: A Functional Perspective and Innovations.International journal of molecular sciences · 2025
    Review
  5. Article
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  7. Review
  8. Article
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  20. Review

53 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

9 authors.

Corinna RichterDepartment of Microbiology and Immunology, University of Otago, PO Box 56, Dunedin 9054, New Zealand.
Ron L DyDepartment of Microbiology and Immunology, University of Otago, PO Box 56, Dunedin 9054, New Zealand.
Rebecca E McKenzieDepartment of Microbiology and Immunology, University of Otago, PO Box 56, Dunedin 9054, New Zealand.
Bridget N J WatsonDepartment of Microbiology and Immunology, University of Otago, PO Box 56, Dunedin 9054, New Zealand.
Corinda TaylorDepartment of Microbiology and Immunology, University of Otago, PO Box 56, Dunedin 9054, New Zealand.
James T ChangDepartment of Microbiology and Immunology, University of Otago, PO Box 56, Dunedin 9054, New Zealand.
Matthew B McNeilDepartment of Microbiology and Immunology, University of Otago, PO Box 56, Dunedin 9054, New Zealand.
Raymond H J StaalsDepartment of Microbiology and Immunology, University of Otago, PO Box 56, Dunedin 9054, New Zealand.
Peter C FineranDepartment of Microbiology and Immunology, University of Otago, PO Box 56, Dunedin 9054, New Zealand peter.fineran@otago.ac.nz.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Clustered regularly interspaced short palindromic repeats (CRISPR), in combination with CRISPR associated (cas) genes, constitute CRISPR-Cas bacterial adaptive immune systems. To generate immunity, these systems acquire short sequences of nucleic acids from foreign invaders and incorporate these into their CRISPR arrays as spacers. This adaptation process is the least characterized step in CRISPR-Cas immunity. Here, we used Pectobacterium atrosepticum to investigate adaptation in Type I-F CRISPR-Cas systems. Pre-existing spacers that matched plasmids stimulated hyperactive primed acquisition and resulted in the incorporation of up to nine new spacers across all three native CRISPR arrays. Endogenous expression of the cas genes was sufficient, yet required, for priming. The new spacers inhibited conjugation and transformation, and interference was enhanced with increasing numbers of new spacers. We analyzed ∼ 350 new spacers acquired in priming events and identified a 5'-protospacer-GG-3' protospacer adjacent motif. In contrast to priming in Type I-E systems, new spacers matched either plasmid strand and a biased distribution, including clustering near the primed protospacer, suggested a bi-directional translocation model for the Cas1:Cas2-3 adaptation machinery. Taken together these results indicate priming adaptation occurs in different CRISPR-Cas systems, that it can be highly active in wild-type strains and that the underlying mechanisms vary.

Indexed as

Clustered Regularly Interspaced Short Palindromic RepeatsCRISPR-Cas SystemsConjugation, GeneticCRISPR-Associated ProteinsPectobacteriumPlasmidsTransformation, GeneticCRISPR-Associated Proteins

Identifiers

PMID24990370
PMCPMC4117759

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LicenceCC BY
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Registered trials

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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.