Vibrio cholerae motility exerts drag force to impede attack by the bacterial predator Bdellovibrio bacteriovorus

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...

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Veröffentlicht in:Nature communications 2018-11, Vol.9 (1), p.4757-9, Article 4757
Hauptverfasser: Duncan, Miles C., Forbes, John C., Nguyen, Y, Shull, Lauren M., Gillette, Rebecca K., Lazinski, David W., Ali, Afsar, Shanks, Robert M. Q., Kadouri, Daniel E., Camilli, Andrew
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Sprache:eng
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Zusammenfassung: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. Prey bacteria have evolved different strategies to counteract predation but the genetic basis remains unclear. Here, Duncan et al. identify key genes involved in Vibrio cholerae sensitivity to Bdellovibrio bacteriovorus predation, providing new insights into prey resistance mechanisms.
ISSN:2041-1723
2041-1723
DOI:10.1038/s41467-018-07245-3