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).

The following data sets were generated

Article and author information

Author details

  1. See-Yeun Ting

    Department of Microbiology, University of Washington, Seattle, United States
    Competing interests
    The authors declare that no competing interests exist.
  2. Kaitlyn D LaCourse

    Department of Microbiology, University of Washington, Seattle, United States
    Competing interests
    The authors declare that no competing interests exist.
  3. Hannah E Ledvina

    Department of Microbiology, University of Washington, Seattle, United States
    Competing interests
    The authors declare that no competing interests exist.
  4. Rutan Zhang

    Department of Medicinal Chemistry, University of Washington, Seattle, United States
    Competing interests
    The authors declare that no competing interests exist.
  5. Matthew C Radey

    Department of Microbiology, University of Washington, Seattle, United States
    Competing interests
    The authors declare that no competing interests exist.
  6. Hemantha D Kulasekara

    Department of Microbiology, University of Washington, Seattle, United States
    Competing interests
    The authors declare that no competing interests exist.
  7. Rahul Somavanshi

    Department of Microbiology, University of Washington, Seattle, United States
    Competing interests
    The authors declare that no competing interests exist.
  8. Savannah K Bertolli

    Department of Microbiology, University of Washington, Seattle, United States
    Competing interests
    The authors declare that no competing interests exist.
  9. Larry A Gallagher

    Department of Microbiology, University of Washington, Seattle, United States
    Competing interests
    The authors declare that no competing interests exist.
  10. Jennifer Kim

    Department of Microbiology, University of Washington, Seattle, United States
    Competing interests
    The authors declare that no competing interests exist.
  11. Kelsi M Penewit

    Department of Laboratory Medicine and Pathology, University of Washington, Seattle, United States
    Competing interests
    The authors declare that no competing interests exist.
  12. Stephen J. Salipante

    Department of Laboratory Medicine and Pathology, University of Washington, Seattle, United States
    Competing interests
    The authors declare that no competing interests exist.
  13. Libin Xu

    Department of Medicinal Chemistry, University of Washington, Seattle, United States
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0003-1021-5200
  14. S Brook Peterson

    Department of Microbiology, University of Washington, Seattle, United States
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0003-2648-0965
  15. Joseph D Mougous

    Department of Microbiology, University of Washington, Seattle, United States
    For correspondence
    mougous@uw.edu
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0002-5417-4861

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.

Reviewing Editor

  1. Tâm Mignot, CNRS-Aix Marseille University, France

Version history

  1. Preprint posted: August 23, 2021 (view preprint)
  2. Received: October 12, 2021
  3. Accepted: February 16, 2022
  4. Accepted Manuscript published: February 17, 2022 (version 1)
  5. Version of Record published: March 16, 2022 (version 2)

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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  1. See-Yeun Ting
  2. Kaitlyn D LaCourse
  3. Hannah E Ledvina
  4. Rutan Zhang
  5. Matthew C Radey
  6. Hemantha D Kulasekara
  7. Rahul Somavanshi
  8. Savannah K Bertolli
  9. Larry A Gallagher
  10. Jennifer Kim
  11. Kelsi M Penewit
  12. Stephen J. Salipante
  13. Libin Xu
  14. S Brook Peterson
  15. Joseph D Mougous
(2022)
Discovery of coordinately regulated pathways that provide innate protection against interbacterial antagonism
eLife 11:e74658.
https://doi.org/10.7554/eLife.74658

Share this article

https://doi.org/10.7554/eLife.74658

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