We are interested in different aspects of cellular aging and organellar connectivity. Using a combination of molecular and cell biology, genetics, biochemistry and imaging, we apply yeast as a model to understand age-associated cellular decay. The causes of aging are intertwined, and interdependent organelle subsystems and networks cooperate to sustain viability. Communication between organelles is ensured by dedicated signal transduction pathways or by direct physical contact at membrane contact sites. We are interested in contact dynamics in response to aging and altered metabolic regimes and the impact of organellar communication on cellular fitness and proteostasis over time.
The capacity of a cell to balance protein synthesis, folding and degradation progressively declines during aging, and long-lived cells are particularly sensitive to the deterioration of protein quality control. The accumulation of abnormal proteins in the course of aging expedites the sequential decay of different proteostatic subsystems maintaining cellular homeostasis, including autophagy. The different projects in our lab are centered around interorganellar communication, facilitated by signal transduction pathways and by direct physical contact between distinct organelles, during aging and in response to altered metabolic regimes.