TY - JOUR
T1 - Inverse regulation of vibrio cholerae biofilm dispersal by polyamine signals
AU - Bridges, Andrew A.
AU - Bassler, Bonnie L.
N1 - Funding Information:
We thank members of the Bassler group and Prof. Ned Wingreen for thoughtful discussions. The c-di-GMP reporter plasmid was a kind gift from Fitnat Yildiz (UC Santa Cruz). Mass spectrometry was conducted by the Princeton Molecular Biology Proteomics and Mass Spectrometry Core Facility. This work was supported by the Howard Hughes Medical Institute, NIH Grant 5R37GM065859, National Science Foundation Grant MCB-1713731, and a Max Planck-Alexander von Humboldt research award to BLB. AAB is a Howard Hughes Medical Institute Fellow of the Damon Runyon Cancer Research Foundation, DRG-2302–17. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Publisher Copyright:
© Bridges and Bassler.
PY - 2021
Y1 - 2021
N2 - 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.
AB - 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.
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U2 - 10.7554/ELIFE.65487
DO - 10.7554/ELIFE.65487
M3 - Article
C2 - 33856344
AN - SCOPUS:85105349342
SN - 2050-084X
VL - 10
JO - eLife
JF - eLife
M1 - e65487
ER -