Prof. Dr Thomas Langer received his PhD in 1993 from the University of Munich after working at the Memorial Sloan Kettering Cancer Center, New York, in the group of F.U. Hartl on mechanisms of chaperone-mediated protein folding. As a postdoctoral researcher he joined the group of W. Neupert at the Department of Physiological Chemistry of the Ludwig-Maximilian-University of Munich and was appointed in 2000 as a full professor at the Institute for Genetics of the University of Cologne. His research interests are mechanisms of mitochondrial quality control and lipid trafficking and their role in neurodegenerative disorders.
A dysfunction of mitochondria, the powerhouses of the cell, has severe cellular consequences and is linked to aging and neurodegeneration. We are interested in cellular surveillance strategies that have evolved to limit mitochondrial damage and ensure cellular integrity. Protein quality control, executed by various intramitochondrial proteases, and the dynamic fusion and fission of mitochondrial membranes are emerging as key processes in the molecular network governing aging and life-span. Impairment of these systems is associated with various neurodegenerative disorders that form the focus of our research. Studies on AAA proteases, energy-dependent quality control enzymes in the inner membrane of mitochondria, and associated prohibitin scaffold complexes have unraveled important regulatory functions for biogenesis and fusion of mitochondrial membranes and highlight the importance of inner membrane integrity for mitochondrial activities and neuronal survival. The stress-induced processing of the dynamin-like GTPase OPA1 by the novel peptidase OMA1 has been identified as a potential sensing mechanism for mitochondrial dysfunction, offering novel approaches for genetic and biochemical interventions.