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RPN-6 determines C. elegans longevity under proteotoxic stress conditions

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  • David Vilchez

    (Howard Hughes Medical Institute, Glenn Center for Aging Research, Molecular and Cell Biology Laboratory, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037, USA)

  • Ianessa Morantte

    (Howard Hughes Medical Institute, Glenn Center for Aging Research, Molecular and Cell Biology Laboratory, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037, USA)

  • Zheng Liu

    (Howard Hughes Medical Institute, Glenn Center for Aging Research, Molecular and Cell Biology Laboratory, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037, USA)

  • Peter M. Douglas

    (Howard Hughes Medical Institute, Glenn Center for Aging Research, Molecular and Cell Biology Laboratory, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037, USA)

  • Carsten Merkwirth

    (Howard Hughes Medical Institute, Glenn Center for Aging Research, Molecular and Cell Biology Laboratory, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037, USA)

  • Ana P. C. Rodrigues

    (Razavi Newman Center for Bioinformatics, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037, USA
    Present addresses: Department of Computational Medicine and Bioinformatics, University of Michigan, 100 Washtenaw Avenue, Ann Arbor, Michigan 48109-2218, USA (A.P.C.R.); Bioinformatics and Computational Biology, Genentech, 1 DNA Way, South San Francisco, California 94080, USA (G.M.).)

  • Gerard Manning

    (Razavi Newman Center for Bioinformatics, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037, USA
    Present addresses: Department of Computational Medicine and Bioinformatics, University of Michigan, 100 Washtenaw Avenue, Ann Arbor, Michigan 48109-2218, USA (A.P.C.R.); Bioinformatics and Computational Biology, Genentech, 1 DNA Way, South San Francisco, California 94080, USA (G.M.).)

  • Andrew Dillin

    (Howard Hughes Medical Institute, Glenn Center for Aging Research, Molecular and Cell Biology Laboratory, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037, USA)

Abstract

Organisms that protect their germ-cell lineages from damage often do so at considerable cost: limited metabolic resources become partitioned away from maintenance of the soma, leaving the ageing somatic tissues to navigate survival amid an environment containing damaged and poorly functioning proteins. Historically, experimental paradigms that limit reproductive investment result in lifespan extension. We proposed that germline-deficient animals might exhibit heightened protection from proteotoxic stressors in somatic tissues. We find that the forced re-investment of resources from the germ line to the soma in Caenorhabditis elegans results in elevated somatic proteasome activity, clearance of damaged proteins and increased longevity. This activity is associated with increased expression of rpn-6, a subunit of the 19S proteasome, by the FOXO transcription factor DAF-16. Ectopic expression of rpn-6 is sufficient to confer proteotoxic stress resistance and extend lifespan, indicating that rpn-6 is a candidate to correct deficiencies in age-related protein homeostasis disorders.

Suggested Citation

  • David Vilchez & Ianessa Morantte & Zheng Liu & Peter M. Douglas & Carsten Merkwirth & Ana P. C. Rodrigues & Gerard Manning & Andrew Dillin, 2012. "RPN-6 determines C. elegans longevity under proteotoxic stress conditions," Nature, Nature, vol. 489(7415), pages 263-268, September.
    • Handle: RePEc:nat:nature:v:489:y:2012:i:7415:d:10.1038_nature11315
    DOI: 10.1038/nature11315
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    1. Atif Ahmed Siddiqui & Emmanuelle Merquiol & Reut Bruck-Haimson & Joud Hirbawi & Hana Boocholez & Irit Cohen & Yonghong Yan & Meng Qiu Dong & Galia Blum & Ehud Cohen, 2024. "Cathepsin B promotes Aβ proteotoxicity by modulating aging regulating mechanisms," Nature Communications, Nature, vol. 15(1), pages 1-14, December.

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