Evidence map›Paper›PMID 27845364›Full record

ArticleScientific reports2016

A genomic island in Vibrio cholerae with VPI-1 site-specific recombination characteristics contains CRISPR-Cas and type VI secretion modules.

Maurizio Labbate, Fabini D Orata, Nicola K Petty, Nathasha D Jayatilleke, William L King, Paul C Kirchberger, Chris Allen, Gulay Mann, Ankur Mutreja, Nicholas R Thomson and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.1field-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

29 citing papers in PubMed, 49 citations in OpenAlex.

  1. Review
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  6. Exploring Mobile Genetic Elements in Vibrio cholerae.Genome biology and evolution · 2025
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  11. Genomic dissection of theMicrobial genomics · 2022
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  14. AMicrobial genomics · 2021
    Article
  15. Article
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  17. Virulence and Antibiotic Resistance Characteristics ofFrontiers in cellular and infection microbiology · 2021
    Article
  18. Article
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  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

12 authors at 4 institutions in 3 countries.

Maurizio LabbateUniversity of Technology Sydney, School of Life Sciences, Sydney, 2007, Australia.
Fabini D OrataUniversity of Alberta, Department of Biological Sciences, Edmonton, T6G 2E9, Canada.
Nicola K PettyUniversity of Technology Sydney, The ithree institute, Sydney, 2007, Australia.
Nathasha D JayatillekeUniversity of Technology Sydney, School of Life Sciences, Sydney, 2007, Australia.
William L KingUniversity of Technology Sydney, School of Life Sciences, Sydney, 2007, Australia.
Paul C KirchbergerUniversity of Alberta, Department of Biological Sciences, Edmonton, T6G 2E9, Canada.
Chris AllenUniversity of Technology Sydney, School of Life Sciences, Sydney, 2007, Australia.
Gulay MannDefence Science and Technology Group, Melbourne, 3207, Australia.
Ankur MutrejaWellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, CB10 1SA, United Kingdom.
Nicholas R ThomsonWellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, CB10 1SA, United Kingdom.
Yan BoucherUniversity of Alberta, Department of Biological Sciences, Edmonton, T6G 2E9, Canada.
Ian G CharlesUniversity of Technology Sydney, The ithree institute, Sydney, 2007, Australia.
University of Technology Sydney · AUUniversity of Alberta · CAWellcome Sanger Institute · GBDefence Science and Technology Group · AU

Funding

Wellcome Trust 098051
6 · The paper itself

Abstract

Cholera is a devastating diarrhoeal disease caused by certain strains of serogroup O1/O139 Vibrio cholerae. Mobile genetic elements such as genomic islands (GIs) have been pivotal in the evolution of O1/O139 V. cholerae. Perhaps the most important GI involved in cholera disease is the V. cholerae pathogenicity island 1 (VPI-1). This GI contains the toxin-coregulated pilus (TCP) gene cluster that is necessary for colonization of the human intestine as well as being the receptor for infection by the cholera-toxin bearing CTX phage. In this study, we report a GI (designated GIVchS12) from a non-O1/O139 strain of V. cholerae that is present in the same chromosomal location as VPI-1, contains an integrase gene with 94% nucleotide and 100% protein identity to the VPI-1 integrase, and attachment (att) sites 100% identical to those found in VPI-1. However, instead of TCP and the other accessory genes present in VPI-1, GIVchS12 contains a CRISPR-Cas element and a type VI secretion system (T6SS). GIs similar to GIVchS12 were identified in other V. cholerae genomes, also containing CRISPR-Cas elements and/or T6SS's. This study highlights the diversity of GIs circulating in natural V. cholerae populations and identifies GIs with VPI-1 recombination characteristics as a propagator of CRISPR-Cas and T6SS modules.

Indexed as

Genomic IslandsBacterial ProteinsClustered Regularly Interspaced Short Palindromic RepeatsMultigene FamilySequence Analysis, DNAType VI Secretion SystemsVibrio cholerae non-O1Vibrio cholerae O139Virulence FactorsBacterial ProteinsType VI Secretion SystemsVirulence Factors

Identifiers

PMID27845364
PMCPMC5109276
OpenAlexW2553304672

What OpenQuestion holds

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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.