Autophagy induction extends lifespan and reduces lipid content in response to frataxin silencing in C. elegans |
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| Authors: | Alfonso Schiavi,Alessandro Torgovnick,Alison Kell,Evgenia Megalou,Natascha Castelein,Ilaria Guccini,Laura Marzocchella,Sara Gelino,Malene Hansen,Florence Malisan,Ivano Condò ,Roberto Bei,Shane L. Rea,Bart P. Braeckman,Nektarios Tavernarakis,Roberto Testi,Natascia Ventura |
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| Affiliation: | 1. Laboratory of Signal Transduction, Department of Biomedicine and Prevention, University of Rome “Tor Vergata”, 00133 Rome, Italy;2. Institute of Clinical Chemistry and Laboratory Medicine of the Heinrich Heine University, and the IUF-Leibniz Research Institute for Environmental Medicine, Duesseldorf, Germany;3. IMBB, Foundation for Research and Technology, Heraklion 71110, Crete, Greece;4. Biology Department, Ghent University, B-9000 Ghent, Belgium;5. Department of Clinical Sciences and Translational Medicine, University of Rome "Tor Vergata", 00133 Rome, Italy;6. Sanford-Burnham Medical Research Institute, Graduate School of Biomedical Sciences, Del E. Webb Neuroscience, Aging and Stem Cell Research Center, Program of Development and Aging, La Jolla, CA, USA;g Sam and Ann Barshop Institute for Longevity and Aging Studies and the Department of Physiology, UTHSCSA, San Antonio, TX, USA |
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| Abstract: | Severe mitochondria deficiency leads to a number of devastating degenerative disorders, yet, mild mitochondrial dysfunction in different species, including the nematode Caenorhabditis elegans, can have pro-longevity effects. This apparent paradox indicates that cellular adaptation to partial mitochondrial stress can induce beneficial responses, but how this is achieved is largely unknown. Complete absence of frataxin, the mitochondrial protein defective in patients with Friedreich's ataxia, is lethal in C. elegans, while its partial deficiency extends animal lifespan in a p53 dependent manner. |
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| Keywords: | Aging Nematode Mitochondria Frataxin p53/cep-1 Autophagy Fat |
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