Individual cells need to adapt to changes in the extracellular environment by altering their intracellular signaling. For example nutrient availability regulates protein synthesis and protein degradation. Other eminent examples for such adaptive responses are the increase and the loss of muscle mass to weight bearing and immobilization, respectively. In the brain, synapses are structurally modified (i.e. strengthened) as a result of high neuronal activity, which underlies learning and memory.

The aim of our studies is to contribute to the better understanding of the molecular mechanisms underlying this cell plasticity in skeletal muscle and the brain. In particular, we will study the role of protein complexes of mTOR (mammalian target of rapamycin), an important signaling hub involved in protein translation, and of the Copines, a family of proteins that mediates calcium-regulated changes in the actin cytoskeleton. As cell plasticity is impaired in several diseases including general muscle wasting, muscular dystrophy, Alzheimer’s disease or autism spectrum disorders, our work may contribute to a better molecular understanding of those diseases and may identify new pathways that might be amenable to interventions.