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Wiley InterScience | ||||||||||||||
  Aging CellSee Also: Volume 6 Issue 1, Pages 95 - 110 Published Online: 5 Dec 2006 Journal compilation © 2010 Blackwell Publishing Ltd/The Anatomical Society of Great Britain and Ireland Published on behalf of the Anatomical Society of Great Britain and Ireland
Abstract | References | Full Text: HTML, PDF (Size: 464K) | Supporting Information | Related Articles | Citation Tracking  Lifespan extension by conditions that inhibit translation in Caenorhabditis elegans Copyright © 2007 The Authors Journal compilation © Blackwell Publishing Ltd/Anatomical Society of Great Britain and Ireland 2007 KEYWORDS aging •
C. elegans
• caloric restriction • insulin/IGF-1 signaling • TOR • translation ABSTRACTMany conditions that shift cells from states of nutrient utilization and growth to states of cell maintenance extend lifespan. We have carried out a systematic lifespan analysis of conditions that inhibit protein synthesis. We find that reducing the levels of ribosomal proteins, ribosomal-protein S6 kinase or translation-initiation factors increases the lifespan of Caenorhabditis elegans. These perturbations, as well as inhibition of the nutrient sensor target of rapamycin (TOR), which is known to increase lifespan, all increase thermal-stress resistance. Thus inhibiting translation may extend lifespan by shifting cells to physiological states that favor maintenance and repair. Interestingly, different types of translation inhibition lead to one of two mutually exclusive outputs, one that increases lifespan and stress resistance through the transcription factor DAF-16/FOXO, and one that increases lifespan and stress resistance independently of DAF-16. Our findings link TOR, but not sir-2.1, to the longevity response induced by dietary restriction (DR) in C. elegans, and they suggest that neither TOR inhibition nor DR extends lifespan simply by reducing protein synthesis. Accepted for publication 14 November 2006 | 
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