Discovery of coordinately regulated pathways that provide innate protection against interbacterial antagonism
Abstract
Bacterial survival is fraught with antagonism, including that deriving from viruses and competing bacterial cells. It is now appreciated that bacteria mount complex antiviral responses; however, whether a coordinated defense against bacterial threats is undertaken is not well understood. Previously we showed that Pseudomonas aeruginosa possess a danger sensing pathway that is a critical fitness determinant during competition against other bacteria. Here, we conducted genome-wide screens in P. aeruginosa that reveal three conserved and widespread interbacterial antagonism resistance clusters (arc1-3). We find that although arc1-3 are coordinately activated by the Gac/Rsm danger sensing system, they function independently and provide idiosyncratic defense capabilities, distinguishing them from general stress response pathways. Our findings demonstrate that Arc3 family proteins provide specific protection against phospholipase toxins by preventing the accumulation of lysophospholipids in a manner distinct from previously characterized membrane repair systems. These findings liken the response of P. aeruginosa to bacterial threats to that of eukaryotic innate immunity, wherein threat detection leads to the activation of specialized defense systems.
Data availability
Sequence data associated with this study is available from the Sequence Read Archive at BioProject PRJNA754428 (http://www.ncbi.nlm.nih.gov/bioproject/754428).
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Author details
Funding
National Institutes of Health (AI080609)
- Joseph D Mougous
National Institutes of Health (DK089507)
- Stephen J. Salipante
National Institutes of Health (R01AI136979)
- Libin Xu
Cystic Fibrosis Foundation (SINGH19R0)
- Stephen J. Salipante
National Institutes of Health (S10OD026741)
- Stephen J. Salipante
Howard Hughes Medical Institute
- Joseph D Mougous
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Copyright
© 2022, Ting et al.
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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