Mitochondria are key organelles mainly devoted to energy production through ATP synthesis. Such a function is permitted by oxidative phosphorylation (OXPHOS) within mitochondria inner membrane. Key components of the OXPHOS processes are encoded by mitochondrial DNA (mtDNA) that is particularly sensitive to exogenous or endogenous insults. As a result, mtDNA mutations are often correlated with OXPHOS dysfunction leading to diseases. ROS production in mitochondria is the main source of mtDNA damage. Such DNA damages are mainly taken over by BER systems within mitochondria. In this study, we focused on this peculiar mitochondrial DNA repair system in Drosophila. In a first step, we analysed in a comprehensive manner through microarray, most glycosylases and endonucleases involved in mitochondrial BER and compared their evolution during aging. Using mutant flies for specific BER enzymes, we started to decipher some of the transcriptional interactions between key BER actors. In a second step, Parp molecule was further studied due its changes in all mutant contexts and for its importance in several cellular processes. We described its nuclear but also its mitochondrial location in S2 cells. Interestingly, two Parp mRNA variants were observed showing distinct regulations following stress induction. However, PARP protein isoforms observed in this study were different compared to what was described in literature. This discrepancy is discussed.
