Our laboratory works with Toxoplasma gondii, an apicomplexan parasite that infects almost one third of the world population. T. gondii also infects animals like cats, dogs, and cattle worldwide. The infection with T. gondii is lifelong and it can cause encephalitis and cardiogenic shock in immune-compromised patients. The infection of pregnant women could result in devastating effect for the unborn fetus. The pathologies associated with toxoplasmosis stem from its lytic cycle, characterized by active invasion, replication inside a parasitophorous vacuole (PV) and egress from host cells causing their lysis. Host cell entry is an obligatory parasite-driven process choreographed by a unique set of proteins that are sequentially released from specific organelles termed micronemes, and rhoptries. Treatment available for toxoplasmosis is not ideal as the available drugs are only effective during the acute disease, and they have harmful side effects after continuous use. A constant source of new drugs and discovery of novel drug targets is needed to stay ahead of the threat posed by this successful pathogen. The lab focuses on two areas of research: 1. Calcium signaling and its impact in each step of the lytic cycle 2. Targeting the mitochondria Left: Lytic cycle of T. gondi. Parasites actively attach and invade host cells, replicate inside a parasitophorous vacuole (PV) and egress lysing the host cell. We can study cytosolic Ca2+ at each step of the lytic cycle with GCaMP6-parasites and host cells expressing RGECO. Clockwise: Motility was stimulated by adding Ca2+. Invasion is observed in a high Ca2+ buffer. Intracell. oscillations were triggered by stimulating host Ca2+ with histamine which does not affect parasite Ca2+. Natural Egress was studied as in Vella S. et al, Cell Calcium, 2021 Right: T. gondii tachyzoites replicating inside a fibroblast cell. Parasites are labeled with a surface marker.