Ubiquinone (Coenzyme Q, CoQ) is present in cells of all tissues but the amount is highly variable. The molecule is an essential component of the mitochondrial electron transport chain. Many reports have demonstrated that CoQ levels are decreased during aging and several diseases as cardiomyopathy, degenerative muscle diseases and cancer. In contrast, its concentration is substantially elevated during neurodegeneration, such as Alzheimer's and prion diseases, and in preneoplastic liver noduli . These findings are likely explained assuming that CoQ is part of the protective cellular response against increased free radicals and reactive metabolites,


Our work focuses on the regulation of CoQ biosynthesis and its antioxidant properties. The biosynthetic biochemical pathway has been outlined both in prokaryotes and eukaryotes, nevertheless little is know about its regulation and integration in the oxidative stress response or energetic metabolism. The main direction of our group is pointing toward assessing roles of uncharacterized genes isolated after genetic analysis of mutants that are defective in ubiquinone synthesis, both in Saccharomyces cerevisiae, Caenorhabditis elegans and human cell lines. Our preliminary data suggest that the phosphorilation state of several CoQ biosynthetic enzymes could have a key role. We are currently investigating the importance of putative mitochondrial kinases in these processes.