We have established the use of Candida albicans, the most common human fungal pathogen, as a new model system to study mitochondrial protein import and biogenesis. This dimorphic yeast provides an excellent system to investigate the coordination of mitochondrial biogenesis with other cellular networks including cellular metabolism and the cell cycle, as it differs substantially from Saccharomyces cerevisiae in its requirements for mitochondrial function in different growth conditions. Assays of radiolabelled protein import into mitochondria isolated from C. albicans have revealed a number of differences in the import and assembly pathways between S. cerevisiae and C. albicans. We examine of the role of the SAM (sorting and assembly machinery) complex in insertion and assembly of mitochondrial outer membrane protein complexes. Import assays combined with analysis of targeting sequences has shown that components of the electron transport chain are imported by distinct pathways in C. albicans and S. cerevisiae, suggesting these pathways can be rewired by evolution to suit the specific needs of an organism. We have also discovered an additional Sam50-like protein in C. albicans, which has enabled us to identify a novel group of Omp85 proteins, the homolog of which has been lost from S. cerevisiae. We suggest that, as a model system for mitochondrial biogenesis, studies of this pathogen will greatly enhance our knowledge of how mitochondria are made and how this is controlled through the course of the cell cycle.