Résumé
Toxoplasma gondii is a unicellular eukaryotic parasite pathogenic to humans. It is the causative agent of toxoplasmosis, an asymptomatic disease in the vast majority of cases, which can be dangerous in immunocompromised patients or in the course of a primary seroconversion in pregnant women. It is considered that the parasite infects one third of the world's population and its transmission is based primarily on the consumption of undercooked meat containing cysts. Cysts represent a form of resistance for the parasite that allows it to evade the host's immune system and persists for its entire life. These forms of resistance are currently inaccessible to therapies. Iron-sulfur clusters are essential cofactors for redox reactions and for the maturation of many essential proteins. Our study model is characterized by the presence of two organelles of endosymbiotic origin: a mitochondrion and a remnant plastid called the apicoplast. In T. gondii we find three metabolic pathways harboring iron- sulfur clusters: the ISC (Iron Sulfur Cluster) pathway harbored within the mitochondria, the CIA (Cytosolic Iron-Sulfur cluster Assembly) pathway in the cytoplasm, and the SUF (Sulfur Utilization Factor) pathway is found in the apicoplast. In the course of our project, we have highlighted the essentiality of several proteins involved in the iron-sulfur clusters biogenesis of the SUF pathway and clarified their function in maintaining the survival of the parasite. The SUF pathway is of particular interest for the discovery of new therapeutic pathways due to its absence in the mammalian host of T. gondii, and its essentiality for the survival of the parasite.