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Nucleolar fibrillarin is an evolutionarily conserved regulator of bacterial pathogen resistance

Author

Listed:
  • Varnesh Tiku

    (Max Planck Institute for Biology of Ageing
    University of Cologne
    Genentech Inc.)

  • Chun Kew

    (Max Planck Institute for Biology of Ageing)

  • Parul Mehrotra

    (Max Planck Institute for Biology of Ageing
    VIB - Ghent University)

  • Raja Ganesan

    (University of Cologne
    University of Cologne)

  • Nirmal Robinson

    (University of Cologne
    University of South Australia)

  • Adam Antebi

    (Max Planck Institute for Biology of Ageing
    University of Cologne)

Abstract

Innate immunity is the first line of defense against infections. Pathways regulating innate responses can also modulate other processes, including stress resistance and longevity. Increasing evidence suggests a role for the nucleolus in regulating cellular processes implicated in health and disease. Here we show the highly conserved nucleolar protein, fibrillarin, is a vital factor regulating pathogen resistance. Fibrillarin knockdown enhances resistance in C. elegans against bacterial pathogens, higher levels of fibrillarin induce susceptibility to infection. Pathogenic infection reduces nucleolar size, ribsosomal RNA, and fibrillarin levels. Genetic epistasis reveals fibrillarin functions independently of the major innate immunity mediators, suggesting novel mechanisms of pathogen resistance. Bacterial infection also reduces nucleolar size and fibrillarin levels in mammalian cells. Fibrillarin knockdown prior to infection increases intracellular bacterial clearance, reduces inflammation, and enhances cell survival. Collectively, these findings reveal an evolutionarily conserved role of fibrillarin in infection resistance and suggest the nucleolus as a focal point in innate immune responses.

Suggested Citation

  • Varnesh Tiku & Chun Kew & Parul Mehrotra & Raja Ganesan & Nirmal Robinson & Adam Antebi, 2018. "Nucleolar fibrillarin is an evolutionarily conserved regulator of bacterial pathogen resistance," Nature Communications, Nature, vol. 9(1), pages 1-10, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-06051-1
    DOI: 10.1038/s41467-018-06051-1
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    Cited by:

    1. Eunah Kim & Andrea Annibal & Yujin Lee & Hae-Eun H. Park & Seokjin Ham & Dae-Eun Jeong & Younghun Kim & Sangsoon Park & Sujeong Kwon & Yoonji Jung & JiSoo Park & Sieun S. Kim & Adam Antebi & Seung-Jae, 2023. "Mitochondrial aconitase suppresses immunity by modulating oxaloacetate and the mitochondrial unfolded protein response," Nature Communications, Nature, vol. 14(1), pages 1-16, December.
    2. Yan-Ping Zhang & Wen-Hong Zhang & Pan Zhang & Qi Li & Yue Sun & Jia-Wen Wang & Shaobing O. Zhang & Tao Cai & Cheng Zhan & Meng-Qiu Dong, 2022. "Intestine-specific removal of DAF-2 nearly doubles lifespan in Caenorhabditis elegans with little fitness cost," Nature Communications, Nature, vol. 13(1), pages 1-18, December.

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