CONICET | Buscador de Institutos y Recursos Humanos

Glucose is the primary source of carbon and energy for the yeast Saccharomyces cerevisiae. Glucose induces glycolytic enzymes and represses the utilization of alternative carbon sources. The Snf1 kinase is a key component of the cellular response to fluctuations in the levels and quality of the carbon source. Its activity is stimulated by glucose limitation, and induces genes that regulate the metabolism of alternative carbon sources, gluconeogenesis and respiration. Taking into account that one of the best known interventions to prolong lifespan is the caloric restriction and that Snf1 is considered a global energy regulator, the aim of this work was to study the participation of Snf1 in cellular longevity. We used strains deficient in the kinases Snf1 and Tor1 and minimal media with carbon sources of different quality. We found that mitochondrial activity of cells lacking SNF1 is higher than in wild type cells grown on non-fermentable carbon sources. All mutant strains grown on a respiratory carbon source are tolerant to oxidative stress. Cells lacking Snf1 and/or Tor1 from a fermentable carbon source at stationary phase are more tolerant to oxidative stress than wild type cells. We found that wild type cells from a strictly respiratory carbon source present a longer chronological lifespan than those from a fermentable carbon source. On caloric restriction growth media, snf1Δ strain is more long-lived than wild type and snf1Δ tor1Δ strains. On restricted carbon sources, there is more autophagy in wild type and snf1 Δtor1Δ cells than in snf1Δ cells. These results indicated that the age-related process, autophagy, is inversely associated with lifespan.