Principal Investigator
Mitochondria are tightly integrated into cellular signalling networks. Major signalling processes are thereby driven by redox molecules. We analyze redox processes and their impact on signalling and on mitochondrial biogenesis.
Redox reactions are at the center of most cellular processes: they are the mechanistic basis of metabolic pathways, they contribute to proteostasis, e.g. by the introduction and removal of disulphide bonds, and they drive the production of reactive oxygen species (ROS), which - with their Janus-faced character of being on the one hand toxic and on the other essential for signalling - impact heavily on cellular physiology. A number of diseases have been directly linked with dysregulated redox homeostasis, including cancer, neurological disorders, cardiovascular diseases, obesity and metabolic diseases, as well as aging.
Redox processes are at the core of most cellular processes and we aim to understand their contribution to the regulation and flawless functionality of these processes
We have characterized novel pathways for protein import into the mitochondrial intermembrane space, and we have investigated the crosstalk of mitochondrial protein import, redox regulation, and metabolic processes in the intermembrane space.
Our goal is to understand in molecular detail the mechanisms and regulation of mitochondrial biogenesis and mitochondrial communication with the remainder of the cell. We aim to understand in molecular detail:
We employ a combination of biochemical and cell biological methods ranging from in vitro reconstitution experiments of whole enzymatic cascades, via different proteomics approaches to tackle specific redox changes and complex assembly processes, genetic screens using CRISPR-Cas technology, to the application of genetically encoded sensors and engineering tools. As model systems, we rely on mammalian cell culture, on mice and baker’s yeast.
Principal Investigator