This laboratory studies the molecular pathogenesis of Toxoplasma gondii infection. Clinical toxoplasmosis in AIDS patients is due to the reactivation of latent bradyzoite forms. They use a variety of cell biology and molecular genetic approaches to determine the mechanism by which T. gondii parasites switch from the rapidly growing tachyzoite form to the latent bradyzoite form. The differentiation of the tachyzoite forms to bradyzoites is a stress-induced differentiation. A major focus of Dr. Kim’s research is identifying the signaling pathways responsible for bradyzoite formation. Their experiments suggest that cyclic nucleotide signaling mediates bradyzoite differentiation and that cAMP-dependent kinase and a GSK-3 family kinase play roles in T. gondii latency. These kinases have been implicated in a variety of other stress-induced differentiation models. Other aspects of the T. gondii stress response are being studied in collaboration with the Weiss laboratory (See below). Approaches being used include knocking out bradyzoite-specific genes and analysis of expression of bradyzoite, cell cycle, and tachyzoite reporter constructs.