Mitochondria, eukaryotic organelles, perform a range of essential tasks in cells, perhaps the best known is ATP production through oxydative phosphorylation. Their dysfunction have been implicated in a number of fatal inherited disorders, in tumorigenesis (Warburg effect), in apoptosis and also as a theoretical cause for ageing. Since this organelle carries a certain number of essential genes in its genome, which is a heavily reduced remnant of its ancestor’s genome, proper synthesis, repair and expression of this mitochondrial DNA (mtDNA) is vital for proper mitochondrial function. A family of DNA-binding proteins, mTERF’s, is drawing increasingly more attention among factors of mitochondrial replication and transcription machineries. Originally named after it first discovered member, a mitochondrial transcription termination factor 1 (mTERF1), their function has been described to be much broader than just transcription termination, extending to mtDNA synthesis, mt gene expression regulation and even mitoribosomal RNA methylation. I have been studying the mTERF1 homologue in Drosophila melanogaster (DmTTF) and found this protein in addition to transcription termination to be essential for coordinating the passage of transcription and replication machineries, regulating the recombination levels of mtDNA and modulating the use of RNA as an intermediate in lagging strand synthesis. However, despite being implicated in a number of essential processes in mt genome maintenance, its precise function and possible association with other members of mtDNA maintenance complex remains elusive. By building on my previous work, I apply for ERMOS postdoctoral grant to study the role of DmTTF in mitochondrial (dys)function in D. melanogaster.