Cellular aging & intracellular communication
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 over time. Communication between organelles is ensured by dedicated signal transduction pathways or by direct physical contact at membrane contact sites (MCS). We are interested in contact dynamics in response to aging, altered metabolic regimes and cell stress and the impact of organellar communication on cellular fitness and proteostasis in aging cells. 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.

Virtually all organelles within a cell are connected by MCS, and such physical interaction facilitates interorganellar communication and the integration of compartmentalized processes by exchange of metabolites, lipids and ions. Moreover, MCS promote the formation of lipid rafts and are associated with misfolded and aggregating proteins. We are interested in MCS dynamics, molecular architecture and abundance in response to aging and cellular stress and the function of MCS in different aspects of proteostasis. In addition, we study how different nutritional regimes, ranging from caloric restriction and phosphate restriction to fermentative vs respiratory carbon sources, affect interorganellar connectivity and organellar function. Our aim is to provide insights into yet unexplored functions of these MCS in cellular homeostasis during aging.

In a national consortium (groups Nyström, Höög, Ott, Andréasson, Büttner), we aim to map how interconnected protein quality control changes genetically, functionally, and structurally during aging and thus affects lifespan, a collaborative project funded by the Knut and Alice Wallenberg foundation.

Keywords
Cellular aging; intracellular communication; membrane contact sites; yeast; proteostasis; autophagy; interconnected quality control; cellular stress; cell death;

Awards and Distinctions
2015 Svenoch Ebba-Christina Hagberg price for important research in cellular aging
2015 Joseph-Krainer Würdigungspreisfor excellent research performance
2008 GE & Science Award, European winner for the best PhD thesis
2008 ÖGGGT award for “Endo G regulates budding yeast life and death”, Mol Cell
2004 Mobbel-price for outstanding diploma thesis
2004 Aventis [i]lab travel grant (Singapore)
2002 DAAD research scholarship (Pakistan)