Mitochondria fulfill important functions in cellular metabolism. The mitochondrial respiratory chain is essential for oxidation phosphorylation and dysfunction can lead to a drastic increase in reactive oxygen species. We showed that increased levels of mitochondria-produced reactive oxygen species result in a fast inhibition of the cytosolic protein synthesis machinery. In project B5, we will study the mechanisms underlying this important intracellular crosstalk and how translation is modulated. Our findings will contribute to a better understanding of mitochondrial dysfunction in human pathologies.