Evidence map›Paper›PMID 26936325›Full record

ArticleCellular microbiology2016

Active and adaptive Legionella CRISPR-Cas reveals a recurrent challenge to the pathogen.

Chitong Rao, Cyril Guyard, Carmen Pelaz, Jessica Wasserscheid, Joseph Bondy-Denomy, Ken Dewar, Alexander W Ensminger

Open access · hybridAbstract read
In one paragraph

Article in Cellular microbiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
4.7field-weighted citation impact, top 6% 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

25 citing papers in PubMed, 37 citations in OpenAlex.

  1. Genomic characterization ofPathogens and global health · 2026
    Article
  2. The discovery of aScience advances · 2025
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  3. Journal of bacteriology · 2024
    Review
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  20. Spacer capture and integration by a type I-F Cas1-Cas2-3 CRISPR adaptation complex.Proceedings of the National Academy of Sciences of the United States of America · 2017
    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

7 authors at 4 institutions in 2 countries.

Chitong RaoDepartment of Molecular Genetics, University of Toronto, Toronto, Ontario, Canada.
Cyril GuyardPublic Health Ontario, Toronto, Ontario, Canada.
Carmen PelazCentro Nacional de Microbiología, Instituto de Salud Carlos III, Madrid, Spain.
Jessica WasserscheidThe McGill University and Génome Québec Innovation Centre, Montreal, Quebec, Canada.
Joseph Bondy-DenomyDepartment of Molecular Genetics, University of Toronto, Toronto, Ontario, Canada.
Ken DewarThe McGill University and Génome Québec Innovation Centre, Montreal, Quebec, Canada.
Alexander W EnsmingerDepartment of Molecular Genetics, University of Toronto, Toronto, Ontario, Canada. alex.ensminger@utoronto.ca.
McGill University and Génome Québec Innovation Centre · CAPublic Health Ontario · CAUniversity of Toronto · CACentro Nacional de Microbiologia · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Clustered regularly interspaced short palindromic repeats with CRISPR-associated gene (CRISPR-Cas) systems are widely recognized as critical genome defense systems that protect microbes from external threats such as bacteriophage infection. Several isolates of the intracellular pathogen Legionella pneumophila possess multiple CRISPR-Cas systems (type I-C, type I-F and type II-B), yet the targets of these systems remain unknown. With the recent observation that at least one of these systems (II-B) plays a non-canonical role in supporting intracellular replication, the possibility remained that these systems are vestigial genome defense systems co-opted for other purposes. Our data indicate that this is not the case. Using an established plasmid transformation assay, we demonstrate that type I-C, I-F and II-B CRISPR-Cas provide protection against spacer targets. We observe efficient laboratory acquisition of new spacers under 'priming' conditions, in which initially incomplete target elimination leads to the generation of new spacers and ultimate loss of the invasive DNA. Critically, we identify the first known target of L. pneumophila CRISPR-Cas: a 30 kb episome of unknown function whose interbacterial transfer is guarded against by CRISPR-Cas. We provide evidence that the element can subvert CRISPR-Cas by mutating its targeted sequences - but that primed spacer acquisition may limit this mechanism of escape. Rather than generally impinging on bacterial fitness, this element drives a host specialization event - with improved fitness in Acanthamoeba but a reduced ability to replicate in other hosts and conditions. These observations add to a growing body of evidence that host range restriction can serve as an existential threat to L. pneumophila in the wild.

Indexed as

Clustered Regularly Interspaced Short Palindromic RepeatsAcanthamoeba castellaniiBase SequenceConserved SequenceEvolution, MolecularGenes, BacterialHost-Pathogen InteractionsLegionella pneumophilaMicrobial ViabilitySequence Analysis, DNA

Identifiers

PMID26936325
PMCPMC5071653
OpenAlexW2292703732

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.