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Activation of the mitochondrial unfolded protein response does not predict longevity in Caenorhabditis elegans

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  • Christopher F. Bennett

    (University of Washington, 1959 NE Pacific Street, D-514, Box 357470, Seattle, Washington 98195-7470, USA
    Molecular and Cellular Biology Program, University of Washington, 1959 NE Pacific Street, Seattle, Washington 98195-7470, USA)

  • Helen Vander Wende

    (University of Washington, 1959 NE Pacific Street, D-514, Box 357470, Seattle, Washington 98195-7470, USA)

  • Marissa Simko

    (University of Washington, 1959 NE Pacific Street, D-514, Box 357470, Seattle, Washington 98195-7470, USA)

  • Shannon Klum

    (University of Washington, 1959 NE Pacific Street, D-514, Box 357470, Seattle, Washington 98195-7470, USA)

  • Sarah Barfield

    (University of Washington, 1959 NE Pacific Street, D-514, Box 357470, Seattle, Washington 98195-7470, USA)

  • Haeri Choi

    (University of Washington, 1959 NE Pacific Street, D-514, Box 357470, Seattle, Washington 98195-7470, USA)

  • Victor V. Pineda

    (University of Washington, 1959 NE Pacific Street, D-514, Box 357470, Seattle, Washington 98195-7470, USA)

  • Matt Kaeberlein

    (University of Washington, 1959 NE Pacific Street, D-514, Box 357470, Seattle, Washington 98195-7470, USA)

Abstract

Recent studies have propagated the model that the mitochondrial unfolded protein response (UPRmt) is causal for lifespan extension from inhibition of the electron transport chain (ETC) in Caenorhabditis elegans. Here we report a genome-wide RNAi screen for negative regulators of the UPRmt. Lifespan analysis of nineteen RNAi clones that induce the hsp-6p::gfp reporter demonstrate differential effects on longevity. Deletion of atfs-1, which is required for induction of the UPRmt, fails to prevent lifespan extension from knockdown of two genes identified in our screen or following knockdown of the ETC gene cco-1. RNAi knockdown of atfs-1 also has no effect on lifespan extension caused by mutation of the ETC gene isp-1. Constitutive activation of the UPRmt by gain of function mutations in atfs-1 fails to extend lifespan. These observations identify several new factors that promote mitochondrial homoeostasis and demonstrate that the UPRmt, as currently defined, is neither necessary nor sufficient for lifespan extension.

Suggested Citation

  • Christopher F. Bennett & Helen Vander Wende & Marissa Simko & Shannon Klum & Sarah Barfield & Haeri Choi & Victor V. Pineda & Matt Kaeberlein, 2014. "Activation of the mitochondrial unfolded protein response does not predict longevity in Caenorhabditis elegans," Nature Communications, Nature, vol. 5(1), pages 1-10, May.
    • Handle: RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms4483
    DOI: 10.1038/ncomms4483
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    1. Silvia Maglioni & Alfonso Schiavi & Marlen Melcher & Vanessa Brinkmann & Zhongrui Luo & Anna Laromaine & Nuno Raimundo & Joel N. Meyer & Felix Distelmaier & Natascia Ventura, 2022. "Neuroligin-mediated neurodevelopmental defects are induced by mitochondrial dysfunction and prevented by lutein in C. elegans," Nature Communications, Nature, vol. 13(1), pages 1-21, December.
    2. Eirini Lionaki & Ilias Gkikas & Ioanna Daskalaki & Maria-Konstantina Ioannidi & Maria I. Klapa & Nektarios Tavernarakis, 2022. "Mitochondrial protein import determines lifespan through metabolic reprogramming and de novo serine biosynthesis," Nature Communications, Nature, vol. 13(1), pages 1-16, December.

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