Mitochondria do not form de novo but derive from preexisting organelles by processes collectively referred to as mitochondrial biogenesis. These include import of most mitochondrial proteins and, in most eukaryotes, import of at least some tRNAs. Furthermore, a limited set of proteins that is essential for oxidative phosphorylation need to be synthesized inside mitochondria. My research group is working on mitochondrial biogenesis using the parasitic protozoa Trypanosoma brucei as a model system. T. brucei belongs to a different eukaryotic supergroup than yeast, mammals and most other model organisms in molecular biology. Its mitochondrion therefore shows many pecularities. The most important ones in the context of our studies are a complete lack of mitochondrial tRNA genes that is compensated by import of cytosolic tRNAs and an apparently minimized mitochondrial protein import system. Moreover, T. brucei is the causative agent of human sleeping sickness and therefore of great clinical importance. Why should research of exotic trypanosome-specific features be of interest for basic science in general? The reason is that these superficially trypanosome-specific features are not really unique, but rather represent extreme examples of processes that in a more cryptic way occur in other cells as well. Thus, most eukaryotes import mitochondrial tRNAs, just not the entire set as T. brucei. All eukaryotes import most of their mitochondrial proteins, however, their import machineries are not as minimized as the one in T. brucei. Thus, T. brucei is an attractive experimentally highly tractable system to study basic as yet poorly understood biological processes.