Labbate, Maurizio, Orata, Fabini D., Petty, Nicola K., Jayatilleke, Nathasha D., King, William L., Kirchberger, Paul C., Allen, Chris, Mann, Gulay, Mutreja, Ankur, Thomson, Nicholas R., Boucher, Yan and Charles, Ian G. (2016) A genomic island in Vibrio cholerae with VPI-1 site-specific recombination characteristics contains CRISPR-Cas and type VI secretion modules. Scientific Reports, 6. ISSN 2045-2322
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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.
Item Type: | Article |
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Uncontrolled Keywords: | general,sdg 3 - good health and well-being ,/dk/atira/pure/subjectarea/asjc/1000 |
Related URLs: | |
Depositing User: | LivePure Connector |
Date Deposited: | 11 Jun 2019 15:30 |
Last Modified: | 14 Dec 2024 01:28 |
URI: | https://ueaeprints.uea.ac.uk/id/eprint/71317 |
DOI: | 10.1038/srep36891 |
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