Project (Peter Rehling)
Mitochondria are essential cellular compartments, associated with a plethora of metabolic processes. Mitochondrial dysfunctions are associated with a heterogeneous group of human disorders characterized by varying clinical symptoms. Moreover, mitochondrial defects have been linked to neurodegeneration (Alzheimer- and Parkinson disease), diabetes, and cancer. It is increasingly evident that besides their metabolic function, mitochondria also represent cellular signaling hubs and thereby regulate various cellular signaling pathways, impacting numerous cellular functions. Accordingly, an active crosstalk between mitochondria and the cellular context is in place but remains largely enigmatic.
In this project, we investigate the communication between mitochondria and their cellular environment during mitochondrial dysfunction. Initial transcriptome analyses of cells defective in respiratory chain complex IV biogenesis has defined a transcriptional response in nuclear gene expression. The central question of this project is to define how the expression of nuclear-encoded mitochondrial proteins changes during mitochondrial dysfunction and which proteins are involved in these signaling pathways. For this, we will combine biochemical approaches with quantitative mass spectrometry and transcriptome analyses to eventually understand how mitochondria regulate cellular functions and vice versa.
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https://biochemie.uni-goettingen.de/index.php?id=379For more information see for instance: