Inverse regulation of Vibrio cholerae biofilm dispersal by polyamine signals
Abstract
The global pathogen Vibrio cholerae undergoes cycles of biofilm formation and dispersal in the environment and the human host. Little is understood about biofilm dispersal. Here, we show that MbaA, a periplasmic polyamine sensor, and PotD1, a polyamine importer, regulate V. cholerae biofilm dispersal. Spermidine, a commonly produced polyamine, drives V. cholerae dispersal, whereas norspermidine, an uncommon polyamine produced by vibrios, inhibits dispersal. Spermidine and norspermidine differ by one methylene group. Both polyamines control dispersal via MbaA detection in the periplasm and subsequent signal relay. Our results suggest that dispersal fails in the absence of PotD1 because endogenously produced norspermidine is not reimported, periplasmic norspermidine accumulates, and it stimulates MbaA signaling. These results suggest that V. cholerae uses MbaA to monitor environmental polyamines, blends of which potentially provide information about numbers of 'self' and 'other'. This information is used to dictate whether or not to disperse from biofilms.
Data availability
All data generated and analyzed in this study are included in the manuscript and supporting files. Source data files have been provided in Zenodo (https://doi.org/10.5281/zenodo.4651348).
Article and author information
Author details
Funding
Howard Hughes Medical Institute (NA)
- Bonnie L Bassler
National Institutes of Health (5R37GM065859)
- Bonnie L Bassler
National Science Foundation (MCB-1713731)
- Bonnie L Bassler
Alexander von Humboldt-Stiftung (NA)
- Bonnie L Bassler
Damon Runyon Cancer Research Foundation (DRG-2302-17)
- Andrew A Bridges
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Copyright
© 2021, Bridges & Bassler
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
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