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KLF-1 orchestrates a xenobiotic detoxification program essential for longevity of mitochondrial mutants

Author

Listed:
  • Marija Herholz

    (University of Cologne)

  • Estela Cepeda

    (University of Cologne)

  • Linda Baumann

    (University of Cologne)

  • Alexandra Kukat

    (University of Cologne)

  • Johannes Hermeling

    (University of Cologne)

  • Sarah Maciej

    (University of Cologne)

  • Karolina Szczepanowska

    (University of Cologne)

  • Victor Pavlenko

    (University of Cologne)

  • Peter Frommolt

    (University of Cologne)

  • Aleksandra Trifunovic

    (University of Cologne
    Center for Molecular Medicine Cologne (CMMC))

Abstract

Most manipulations that extend lifespan also increase resistance to various stress factors and environmental cues in a range of animals from yeast to mammals. However, the underlying molecular mechanisms regulating stress resistance during aging are still largely unknown. Here we identify Krüppel-like factor 1 (KLF-1) as a mediator of a cytoprotective response that dictates longevity induced by reduced mitochondrial function. A redox-regulated KLF-1 activation and transfer to the nucleus coincides with the peak of somatic mitochondrial biogenesis that occurs around a transition from larval stage L3 to D1. We further show that KLF-1 activates genes involved in the xenobiotic detoxification programme and identified cytochrome P450 oxidases, the KLF-1 main effectors, as longevity-assurance factors of mitochondrial mutants. Collectively, these findings underline the importance of the xenobiotic detoxification in the mitohormetic, longevity assurance pathway and identify KLF-1 as a central factor in orchestrating this response.

Suggested Citation

  • Marija Herholz & Estela Cepeda & Linda Baumann & Alexandra Kukat & Johannes Hermeling & Sarah Maciej & Karolina Szczepanowska & Victor Pavlenko & Peter Frommolt & Aleksandra Trifunovic, 2019. "KLF-1 orchestrates a xenobiotic detoxification program essential for longevity of mitochondrial mutants," Nature Communications, Nature, vol. 10(1), pages 1-15, December.
    • Handle: RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-11275-w
    DOI: 10.1038/s41467-019-11275-w
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