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Proc Natl Acad Sci U S A. 2015 Aug 25;112(34):10798-803. doi: 10.1073/pnas.1503129112. Epub 2015 Aug 10.

The opportunistic marine pathogen Vibrio parahaemolyticus becomes virulent by acquiring a plasmid that expresses a deadly toxin.

Author information

1
Institute of Bioinformatics and Biosignal Transduction, College of Bioscience and Biotechnology, National Cheng Kung University, Tainan 701, Taiwan; Department of Microbiology and Immunology, College of Medicine, National Cheng Kung University, Tainan 701, Taiwan;
2
Institute of Bioinformatics and Biosignal Transduction, College of Bioscience and Biotechnology, National Cheng Kung University, Tainan 701, Taiwan; Department of Life Science, National Taiwan University, Taipei 104, Taiwan;
3
Institute of Biological Chemistry, Academia Sinica, Taipei 115, Taiwan;
4
Institute of Bioinformatics and Biosignal Transduction, College of Bioscience and Biotechnology, National Cheng Kung University, Tainan 701, Taiwan;
5
Graduate Institute of Translational Medicine, College of Medical Science and Technology, Taipei Medical University, Taipei 110, Taiwan;
6
Genome and Systems Biology Degree Program, National Taiwan University and Academia Sinica, Taipei 115, Taiwan; Department of Bio-Industrial Mechatronics Engineering, National Taiwan University, Taipei 104, Taiwan;
7
Institute of Biotechnology, National Taiwan University, Taipei 104, Taiwan;
8
Aquaculture Pathology Laboratory, School of Animal and Comparative Biomedical Sciences, University of Arizona, Tucson, AZ 85721;
9
Institute of Biotechnology, College of Bioscience and Biotechnology, National Cheng Kung University, Tainan 701, Taiwan;
10
Graduate Institute of Translational Medicine, College of Medical Science and Technology, Taipei Medical University, Taipei 110, Taiwan; gracelow@mail.ncku.edu.tw h061453@mail.ncku.edu.tw wanghc@tmu.edu.tw.
11
Department of Microbiology and Immunology, College of Medicine, National Cheng Kung University, Tainan 701, Taiwan; gracelow@mail.ncku.edu.tw h061453@mail.ncku.edu.tw wanghc@tmu.edu.tw.
12
Institute of Bioinformatics and Biosignal Transduction, College of Bioscience and Biotechnology, National Cheng Kung University, Tainan 701, Taiwan; Department of Life Science, National Taiwan University, Taipei 104, Taiwan; Center of Bioscience and Biotechnology, National Cheng Kung University, Tainan 701, Taiwan gracelow@mail.ncku.edu.tw h061453@mail.ncku.edu.tw wanghc@tmu.edu.tw.

Abstract

Acute hepatopancreatic necrosis disease (AHPND) is a severe, newly emergent penaeid shrimp disease caused by Vibrio parahaemolyticus that has already led to tremendous losses in the cultured shrimp industry. Until now, its disease-causing mechanism has remained unclear. Here we show that an AHPND-causing strain of V. parahaemolyticus contains a 70-kbp plasmid (pVA1) with a postsegregational killing system, and that the ability to cause disease is abolished by the natural absence or experimental deletion of the plasmid-encoded homologs of the Photorhabdus insect-related (Pir) toxins PirA and PirB. We determined the crystal structure of the V. parahaemolyticus PirA and PirB (PirA(vp) and PirB(vp)) proteins and found that the overall structural topology of PirA(vp)/PirB(vp) is very similar to that of the Bacillus Cry insecticidal toxin-like proteins, despite the low sequence identity (<10%). This structural similarity suggests that the putative PirAB(vp) heterodimer might emulate the functional domains of the Cry protein, and in particular its pore-forming activity. The gene organization of pVA1 further suggested that pirAB(vp) may be lost or acquired by horizontal gene transfer via transposition or homologous recombination.

KEYWORDS:

AHPND; Pir toxin; Vibrio parahaemolyticus; shrimp; virulence plasmid

PMID:
26261348
PMCID:
PMC4553777
DOI:
10.1073/pnas.1503129112
[Indexed for MEDLINE]
Free PMC Article

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