“Mighty-chondria”

Why are they worthy of their name?

Our aim is to decipher the role of mitochondria as main regulators of signaling transductions, especially in the case of OXPHOS dysfunction. When mitochondria experience stress or when dysfunction occurs, the organelle sends signals to the nucleus, which launches different types of adaptive responses. Transcription factors are activated and stimulate the expression of specific sets of genes, whose products enable the cell to adapt to the changes. We aim to further understand these largely unknown mechanisms that play a central role in determining the extent of tissue specific defect arising from the respiratory chain deficiency. The primary focus of our research is in deciphering the precise signaling cascade of the pathogenic mechanisms leading to mitochondrial diseases and ageing, with the ultimate goal of identifying new therapeutic targets and strategies.

The group mainly uses in vivo model systems: multiple transgenic mouse models and roundworm Caenorhabditis elegans to tackle specific questions of mitochondrial pathophysiology. Many of the transgenic mice models are developed within the group, most recently using the CRISPR/Cas9 techniques. The group relies on various molecular biology techniques to understand the complex signaling pathways, many of which are specifically developed to understand the mitochondrial physiology. To tackle complex molecular mechanisms of specific processes in details, we often turn to mammalian cell-based models and different biochemical approaches.