Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 113, Issue 22, Pages 6283-6288Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1601718113
Keywords
Vibrio parahaemolyticus; transposon-insertion sequencing; type III secretion; bacterial pathogenesis; pathogen evolution
Categories
Funding
- NIH [R37 AI-042347, F31 AI-120665, F32 GM108355-02]
- Howard Hughes Medical Institute
- Northern Norway Regional Health Authority [SFP1293-16, A67600]
- Research Council of Norway [249979/RU]
- Bill & Melinda Gates Foundation [OPP1111658]
- Pew Latin American Fellowship
- Becas Chile Postdoctoral Fellowship
- Bill and Melinda Gates Foundation [OPP1111658] Funding Source: Bill and Melinda Gates Foundation
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Vibrio parahaemolyticus is the most common cause of seafood-borne gastroenteritis worldwide and a blight on global aquaculture. This organism requires a horizontally acquired type III secretion system (T3SS2) to infect the small intestine, but knowledge of additional factors that underlie V. parahaemolyticus pathogenicity is limited. We used transposon-insertion sequencing to screen for genes that contribute to viability of V. parahaemolyticus in vitro and in the mammalian intestine. Our analysis enumerated and controlled for the host infection bottleneck, enabling robust assessment of genetic contributions to in vivo fitness. We identified genes that contribute to V. parahaemolyticus colonization of the intestine independent of known virulence mechanisms in addition to uncharacterized components of T3SS2. Our study revealed that toxR, an ancestral locus in Vibrio species, is required for V. parahaemolyticus fitness in vivo and for induction of T3SS2 gene expression. The regulatory mechanism by which V. parahaemolyticus ToxR activates expression of T3SS2 resembles Vibrio cholerae ToxR regulation of distinct virulence elements acquired via lateral gene transfer. Thus, disparate horizontally acquired virulence systems have been placed under the control of this ancestral transcription factor across independently evolved human pathogens.
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