Author
Listed:
- Miles C. Duncan
(Tufts University School of Medicine)
- John C. Forbes
(Harvard-Smithsonian Center for Astrophysics)
- Y Nguyen
(Tufts University School of Medicine
University of Texas Southwestern Medical Center)
- Lauren M. Shull
(Tufts University School of Medicine)
- Rebecca K. Gillette
(Tufts University School of Medicine)
- David W. Lazinski
(Tufts University School of Medicine)
- Afsar Ali
(University of Florida
University of Florida)
- Robert M. Q. Shanks
(University of Pittsburgh)
- Daniel E. Kadouri
(Rutgers School of Dental Medicine)
- Andrew Camilli
(Tufts University School of Medicine)
Abstract
The bacterial predator Bdellovibrio bacteriovorus is evolved to attack and kill other bacteria, including the human intestinal pathogen Vibrio cholerae. Although B. bacteriovorus exhibit a broad prey range, little is known about the genetic determinants of prey resistance and sensitivity. Here we perform a genetic screen on V. cholerae and identify five pathways contributing to predation susceptibility. We find that the essential virulence regulators ToxR/S increase susceptibility to predation, as mutants of these genes are more resistant to predation. We observe by flow cytometry that lipopolysaccharide is a critical defense, as mutants lacking O-antigen are rapidly attacked by predatory B. bacteriovorus. Using polymer solutions to alter media viscosity, we find that when B. bacteriovorus attacks motile V. cholerae, increased drag forces slow its ability to prey. These results provide insights into key prey resistance mechanisms, and may be useful in the application of B. bacteriovorus in treating infections.
Suggested Citation
Miles C. Duncan & John C. Forbes & Y Nguyen & Lauren M. Shull & Rebecca K. Gillette & David W. Lazinski & Afsar Ali & Robert M. Q. Shanks & Daniel E. Kadouri & Andrew Camilli, 2018.
"Vibrio cholerae motility exerts drag force to impede attack by the bacterial predator Bdellovibrio bacteriovorus,"
Nature Communications, Nature, vol. 9(1), pages 1-9, December.
Handle:
RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-07245-3
DOI: 10.1038/s41467-018-07245-3
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