In most eukaryotes, mitochondrial membrane potential is essential for survival. This potential is generated by the proton pumping across the inner mitochondrial membrane initiated by electron transfer from ubiquinol to cytochrome c. Collapse of membrane potential can stimulate apoptosis. Our lab investigates the mechanism by which Atovaquone, an antimalarial, collapses this potential. I am determining if treatment with Atovaquone alters the overall gene expression of Plasmodium falciparum and ultimately leads to its demise. Preliminary experiments suggest that these parasites can survive up to 48h with a collapsed membrane potential. Future experiments will further determine if this survival is stage-specific and what, if any, gene expression is altered.