Nutrient sensing and organelle communication in the parasites casing toxoplasmosis and malaria

Toxoplasma parasites cause death of babies and AIDS patients. Plasmodium spp, causes malaria. Both parasites go through several stages during their infection and dissemination of a human. All stages must invade cells of their host to survive and when resources run out in one cell they must survive extracellularly until they find the next cell. Surviving extracellularly and replicating intracellularly are thus essential aspects of these parasite's virulence. Intricate connection with the environment allows these parasites to sense nutrient availability and to decide whether to replicate or to disseminate and transmit.
Mitochondria and plastids are the main metabolic centres in these parasites and they have unique pathways that utilized scavenged materials from the host cell to provide the energy and lipid needed in the various life stages. These functions are essential and some of them are confirmed sources for drug targets, including the target of Atovaquone, for which the spread of drug resistance is unlikely.
In this project we will explore how the organelles responsible for energy and lipid metabolism communicate with each other and with other organelles within the parasite to respond to change in nutrient availability and to determines cell fate. We will focus on glucose and lipid sensing pathways and on exchange of molecules between mitochondrion and plastid. For this we will combine reverse genetics, drug screening, metabolomics and imaging approaches in vitro in Toxoplasma and in Plasmodium.