Microsporidia are a group of parasites that infect animals and immunocompromised humans. In infected individuals, they cause severe diseases, like encephalitis (inflammation of the brain) and gastroenteritis (inflammation of the stomach). As organisms that are dependent upon their host for survival, some of the microsporidia’s organelles (internal structures) and metabolic functions are missing or deficient in comparison to other single-celled organisms. One example is the mitochondrion, an organelle that normally contains many enzymes important for cell metabolism, including those responsible for the conversion of sugar to usable energy. A highly reduced relic of the mitochondrion was recently discovered in microsporidia. The role and metabolic function of this deficient organelle remain unclear. Dr. Lena Burri’s research project is to identify and characterize proteins that are imported into the mitochondrion, how these proteins are directed to their final destination and in which metabolic pathway they are involved. Understanding the function of the relic mitochondria in microsporidia may provide ways to combat these organisms, as mitochondrial functions are important potential drug targets.