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Mucin induces CRISPR-Cas defense in an opportunistic pathogen

Author

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  • Gabriel Magno Freitas Almeida

    (University of Jyväskylä, Department of Biological and Environmental Science and Nanoscience Center
    UiT The Arctic University of Norway)

  • Ville Hoikkala

    (University of Jyväskylä, Department of Biological and Environmental Science and Nanoscience Center)

  • Janne Ravantti

    (University of Helsinki, Molecular and Integrative Biosciences Research Programme)

  • Noora Rantanen

    (University of Jyväskylä, Department of Biological and Environmental Science and Nanoscience Center)

  • Lotta-Riina Sundberg

    (University of Jyväskylä, Department of Biological and Environmental Science and Nanoscience Center)

Abstract

Parasitism by bacteriophages has led to the evolution of a variety of defense mechanisms in their host bacteria. However, it is unclear what factors lead to specific defenses being deployed upon phage infection. To explore this question, we co-evolved the bacterial fish pathogen Flavobacterium columnare and its virulent phage V156 in presence and absence of a eukaryotic host signal (mucin) for sixteen weeks. The presence of mucin leads to a dramatic increase in CRISPR spacer acquisition, especially in low nutrient conditions where over 60% of colonies obtain at least one new spacer. Additionally, we show that the presence of a competitor bacterium further increases CRISPR spacer acquisition in F. columnare. These results suggest that ecological factors are important in determining defense strategies against phages, and that the phage-bacterium interactions on mucosal surfaces may select for the diversification of bacterial immune systems.

Suggested Citation

  • Gabriel Magno Freitas Almeida & Ville Hoikkala & Janne Ravantti & Noora Rantanen & Lotta-Riina Sundberg, 2022. "Mucin induces CRISPR-Cas defense in an opportunistic pathogen," Nature Communications, Nature, vol. 13(1), pages 1-12, December.
  • Handle: RePEc:nat:natcom:v:13:y:2022:i:1:d:10.1038_s41467-022-31330-3
    DOI: 10.1038/s41467-022-31330-3
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    References listed on IDEAS

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    1. Ellinor O. Alseth & Elizabeth Pursey & Adela M. Luján & Isobel McLeod & Clare Rollie & Edze R. Westra, 2019. "Bacterial biodiversity drives the evolution of CRISPR-based phage resistance," Nature, Nature, vol. 574(7779), pages 549-552, October.
    2. Timothy R. Sampson & Sunil D. Saroj & Anna C. Llewellyn & Yih-Ling Tzeng & David S. Weiss, 2013. "A CRISPR/Cas system mediates bacterial innate immune evasion and virulence," Nature, Nature, vol. 497(7448), pages 254-257, May.
    3. Timothy R. Sampson & Sunil D. Saroj & Anna C. Llewellyn & Yih-Ling Tzeng & David S. Weiss, 2013. "Correction: Corrigendum: A CRISPR/Cas system mediates bacterial innate immune evasion and virulence," Nature, Nature, vol. 501(7466), pages 262-262, September.
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    5. Elina Laanto & Ville Hoikkala & Janne Ravantti & Lotta-Riina Sundberg, 2017. "Long-term genomic coevolution of host-parasite interaction in the natural environment," Nature Communications, Nature, vol. 8(1), pages 1-8, December.
    6. Alexander J. Meeske & Sandra Nakandakari-Higa & Luciano A. Marraffini, 2019. "Cas13-induced cellular dormancy prevents the rise of CRISPR-resistant bacteriophage," Nature, Nature, vol. 570(7760), pages 241-245, June.
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    1. Eleri A. Ashworth & Rosanna C. T. Wright & Rebecca K. Shears & Janet K. L. Wong & Akram Hassan & James P. J. Hall & Aras Kadioglu & Joanne L. Fothergill, 2024. "Exploiting lung adaptation and phage steering to clear pan-resistant Pseudomonas aeruginosa infections in vivo," Nature Communications, Nature, vol. 15(1), pages 1-16, December.

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