C. elegans longevity pathways converge to decrease mitochondrial membrane potential
| Autor: | Dana Gášková, Bernard D. Lemire, Maciej Behrendt, Adrienne DeCorby |
|---|---|
| Rok vydání: | 2009 |
| Předmět: |
Membrane Potential
Mitochondrial Membrane potential Carbonyl Cyanide m-Chlorophenyl Hydrazone Aging Bioenergetics biology Uncoupling Agents Longevity Wild type Oxidative phosphorylation Mitochondrion biology.organism_classification Mitochondria Cell biology Mitochondrial Proteins Animals Inner membrane Signal transduction Caenorhabditis elegans Caenorhabditis elegans Proteins Developmental Biology |
| Zdroj: | Mechanisms of Ageing and Development. 130:461-465 |
| ISSN: | 0047-6374 |
| DOI: | 10.1016/j.mad.2009.05.001 |
| Popis: | Energy production via oxidative phosphorylation generates a mitochondrial membrane potential (DeltaPsi(m)) across the inner membrane. In this work, we show that a lower DeltaPsi(m) is associated with increased lifespan in Caenorhabditis elegans. The long-lived mutants daf-2(e1370), age-1(hx546), clk-1(qm30), isp-1(qm150) and eat-2(ad465) all have a lower DeltaPsi(m) than wild type animals. The lower DeltaPsi(m) of daf-2(e1370) is daf-16 dependent, indicating that the insulin-like signaling pathway not only regulates lifespan but also mitochondrial energetics. RNA interference (RNAi) against 17 genes shown to extend lifespan also decrease DeltaPsi(m). Furthermore, lifespan can be significantly extended with the uncoupler carbonylcyanide-3-chlorophenylhydrazone (CCCP), which dissipates DeltaPsi(m). We conclude that longevity pathways converge on the mitochondria and lead to a decreased DeltaPsi(m). Our results are consistent with the 'uncoupling to survive' hypothesis, which states that dissipation of the DeltaPsi(m) will extend lifespan. |
| Databáze: | OpenAIRE |
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