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DNA damage in germ cells induces an innate immune response that triggers systemic stress resistance

Author

Listed:
  • Maria A. Ermolaeva

    (Cologne Excellence Cluster for Cellular Stress Responses in Aging-Associated Diseases (CECAD), Institute for Genetics, University of Cologne, Zülpicher Strasse 47a, 50674 Cologne, Germany)

  • Alexandra Segref

    (Cologne Excellence Cluster for Cellular Stress Responses in Aging-Associated Diseases (CECAD), Institute for Genetics, University of Cologne, Zülpicher Strasse 47a, 50674 Cologne, Germany)

  • Alexander Dakhovnik

    (Cologne Excellence Cluster for Cellular Stress Responses in Aging-Associated Diseases (CECAD), Institute for Genetics, University of Cologne, Zülpicher Strasse 47a, 50674 Cologne, Germany)

  • Hui-Ling Ou

    (Cologne Excellence Cluster for Cellular Stress Responses in Aging-Associated Diseases (CECAD), Institute for Genetics, University of Cologne, Zülpicher Strasse 47a, 50674 Cologne, Germany)

  • Jennifer I. Schneider

    (Cologne Excellence Cluster for Cellular Stress Responses in Aging-Associated Diseases (CECAD), Institute for Genetics, University of Cologne, Zülpicher Strasse 47a, 50674 Cologne, Germany)

  • Olaf Utermöhlen

    (Institute for Medical Microbiology, Immunology and Hygiene, Medical Center, University of Cologne, Goldenfelsstrasse 19-21, 50935 Cologne, Germany
    Center for Molecular Medicine Cologne (CMMC), University of Cologne, 50931 Cologne, Germany)

  • Thorsten Hoppe

    (Cologne Excellence Cluster for Cellular Stress Responses in Aging-Associated Diseases (CECAD), Institute for Genetics, University of Cologne, Zülpicher Strasse 47a, 50674 Cologne, Germany)

  • Björn Schumacher

    (Cologne Excellence Cluster for Cellular Stress Responses in Aging-Associated Diseases (CECAD), Institute for Genetics, University of Cologne, Zülpicher Strasse 47a, 50674 Cologne, Germany
    Systems Biology of Ageing Cologne, University of Cologne, 50937 Cologne, Germany)

Abstract

In Caenorhabditis elegans, genome instability in the form of exogenous and endogenous DNA damage in germ cells evokes elevated heat- and oxidative-stress resistance in somatic tissues; this is mediated by MPK-1, which triggers the induction of putative secreted peptides associated with innate immunity, leading to activation of the ubiquitin–proteasome system.

Suggested Citation

  • Maria A. Ermolaeva & Alexandra Segref & Alexander Dakhovnik & Hui-Ling Ou & Jennifer I. Schneider & Olaf Utermöhlen & Thorsten Hoppe & Björn Schumacher, 2013. "DNA damage in germ cells induces an innate immune response that triggers systemic stress resistance," Nature, Nature, vol. 501(7467), pages 416-420, September.
    • Handle: RePEc:nat:nature:v:501:y:2013:i:7467:d:10.1038_nature12452
    DOI: 10.1038/nature12452
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    Cited by:

    1. Najmeh Soltanmohammadi & Siyao Wang & Björn Schumacher, 2022. "Somatic PMK-1/p38 signaling links environmental stress to germ cell apoptosis and heritable euploidy," Nature Communications, Nature, vol. 13(1), pages 1-13, December.
    2. Liankui Zhou & Liu Jiang & Lan Li & Chengchuan Ma & Peixue Xia & Wanqiu Ding & Ying Liu, 2024. "A germline-to-soma signal triggers an age-related decline of mitochondrial stress response," Nature Communications, Nature, vol. 15(1), pages 1-19, December.

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