1. Microbiology and Infectious Disease

Kin cell lysis is a danger signal that activates antibacterial pathways of Pseudomonas aeruginosa

  1. Michele LeRoux
  2. Robin L Kirkpatrick
  3. Elena I Montauti
  4. Bao Q Tran
  5. S Brook Peterson
  6. Brittany N Harding
  7. John C Whitney
  8. Alistair B Russell
  9. Beth Traxler
  10. Young Ah Goo
  11. David R Goodlett
  12. Paul A Wiggins
  13. Joseph D Mougous  Is a corresponding author
  1. University of Washington, United States
  2. University of Maryland, United States
https://doi.org/10.7554/eLife.05701
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Cite this article
  1. Michele LeRoux
  2. Robin L Kirkpatrick
  3. Elena I Montauti
  4. Bao Q Tran
  5. S Brook Peterson
  6. Brittany N Harding
  7. John C Whitney
  8. Alistair B Russell
  9. Beth Traxler
  10. Young Ah Goo
  11. David R Goodlett
  12. Paul A Wiggins
  13. Joseph D Mougous
(2015)
Kin cell lysis is a danger signal that activates antibacterial pathways of Pseudomonas aeruginosa
eLife 4:e05701.
https://doi.org/10.7554/eLife.05701
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Abstract

The perception and response to cellular death is an important aspect of multicellular eukaryotic life. For example, damage-associated molecular patterns activate an inflammatory cascade that leads to removal of cellular debris and promotion of healing. We demonstrate that lysis of Pseudomonas aeruginosa cells triggers a program in the remaining population that confers fitness in interspecies co-culture. We find that this program, termed P. aeruginosa response to antagonism (PARA), involves rapid deployment of antibacterial factors and is mediated by the Gac/Rsm global regulatory pathway. Type VI secretion, and, unexpectedly, conjugative type IV secretion within competing bacteria, induce P. aeruginosa lysis and activate PARA, thus providing a mechanism for the enhanced capacity of P. aeruginosa to target bacteria that elaborate these factors. Our finding that bacteria sense damaged kin and respond via a widely distributed pathway to mount a complex response raises the possibility that danger sensing is an evolutionarily conserved process.

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Author details

  1. Michele LeRoux

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

  2. Robin L Kirkpatrick

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

  3. Elena I Montauti

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

  4. Bao Q Tran

    Department of Pharmaceutical Sciences, School of Pharmacy, University of Maryland, Baltimore, United States
    Competing interests
    The authors declare that no competing interests exist.

  5. S Brook Peterson

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

  6. Brittany N Harding

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

  7. John C Whitney

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

  8. Alistair B Russell

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

  9. Beth Traxler

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

  10. Young Ah Goo

    Department of Pharmaceutical Sciences, School of Pharmacy, University of Maryland, Baltimore, United States
    Competing interests
    The authors declare that no competing interests exist.

  11. David R Goodlett

    Department of Pharmaceutical Sciences, School of Pharmacy, University of Maryland, Baltimore, United States
    Competing interests
    The authors declare that no competing interests exist.

  12. Paul A Wiggins

    Department of Physics, University of Washington, Seattle, United States
    Competing interests
    The authors declare that no competing interests exist.

  13. 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.

Reviewing Editor

  1. Michael Laub, Massachusetts Institute of Technology, United States

Version history

  1. Received: November 20, 2014
  2. Accepted: January 30, 2015
  3. Accepted Manuscript published: February 2, 2015 (version 1)
  4. Version of Record published: March 3, 2015 (version 2)

Copyright

© 2015, LeRoux 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. Michele LeRoux
  2. Robin L Kirkpatrick
  3. Elena I Montauti
  4. Bao Q Tran
  5. S Brook Peterson
  6. Brittany N Harding
  7. John C Whitney
  8. Alistair B Russell
  9. Beth Traxler
  10. Young Ah Goo
  11. David R Goodlett
  12. Paul A Wiggins
  13. Joseph D Mougous
(2015)
Kin cell lysis is a danger signal that activates antibacterial pathways of Pseudomonas aeruginosa
eLife 4:e05701.
https://doi.org/10.7554/eLife.05701

Share this article

https://doi.org/10.7554/eLife.05701

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