Lifespan extension by conditions that inhibit translation in <i>Caenorhabditis elegans</i>

Aging Cell - Tập 6 Số 1 - Trang 95-110 - 2007
Malene Hansen1, Stefan Taubert2, Douglas K. Crawford3, Nataliya Libina3, Seung‐Jae Lee3, Cynthia Kenyon3
1Department of Biochemistry and Biophysics, University of California, 600 16th Street, San Francisco, CA 94158, USA.
2Department of Cellular and Molecular Pharmacology, University of California, 600 – 16th Street, San Francisco, CA 94158, USA
3Department of Biochemistry and Biophysics and

Tóm tắt

SummaryMany 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.

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Aging Cell

Tập 6 Số 1

95-110

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