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Research Paper
Longevity pathways converge on autophagy genes to regulate life span in Caenorhabditis elegans
Márton L. Tóth, Tímea Sigmond, Éva Borsos, János Barna, Péter Erdélyi, Krisztina Takács-Vellai, László Orosz, Attila L. Kovács, György Csikós, Miklós Sass and Tibor Vellai
volume 4 | issue 3
1 April 2008Pages: 330 - 338
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Aging is a multifactorial process with many mechanisms contributing to the decline. Mutations decreasing insulin/IGF-1 (insulin-like growth factor-1) or TOR (target of rapamycin) kinase-mediated signaling, mitochondrial activity and food intake each extend life span in divergent animal phyla. Understanding how these genetically distinct mechanisms interact to control longevity is a fundamental and fascinating problem in biology. Here we show that mutational inactivation of autophagy genes, which are involved in the degradation of aberrant, damaged cytoplasmic constituents accumulating in all aging cells, accelerates the rate at which the tissues age in the nematode Caenorhabditis elegans. According to our results Drosophila flies deficient in autophagy are also short-lived. We further demonstrate that reduced activity of autophagy genes suppresses life span extension in mutant nematodes with inherent dietary restriction, aberrant insulin/IGF-1 or TOR signaling, and lowered mitochondrial respiration. These findings suggest that the autophagy gene cascade functions downstream of and is inhibited by different longevity pathways in C. elegans, therefore, their effects converge on autophagy genes to slow down aging and lengthen life span. Thus, autophagy may act as a central regulatory mechanism of animal aging.
Authors
Márton L. Tóth
ELTE University
Tímea Sigmond
Eötvös Loránd University
Éva Borsos
Eötvös Loránd University
János Barna
Eötvös Loránd University
Péter Erdélyi
Eötvös Loránd University
Krisztina Takács-Vellai
Eötvös Loránd University
László Orosz
Eötvös Loránd University
Attila L. Kovács
Eötvös Loránd University
György Csikós
Eötvös Loránd University
Miklós Sass
Eötvös Loránd University
Tibor Vellai
Eötvös Loránd University





