Identification of genes involved in signalling during host cell invasion by the apicomplexan parasite Toxoplasma gondii

• Antragsteller: Dr. Moritz Treeck
• Fachliche Zuordnung: Parasitologie und Biologie der Erreger tropischer Infektionskrankheiten
• Förderung: Förderung von 2009 bis 2011
• Projektkennung: Deutsche Forschungsgemeinschaft (DFG) - Projektnummer 161118571

Apicomplexan parasites possess the ability to invade a variety of host cells using a sophisticated system of adhesion proteins, molecular motors and proteolytic processing events. A range of proteins in these numerous species provides specificity for different parasite-host combinations but a number of proteins that are involved in the invasion process are conserved across the phylum. Most of the latter proteins are stored in secretory organelles called rhoptries and micronemes, secretion from which is associated with release of intracellular calcium stores as well as changes in cAMP levels. Importantly, the signals that lead to calcium and cAMP signalling and the downstream effects on invasion are not known. The goal of the project I propose here is to identify the signalling molecules that are involved in rhoptry/microneme secretion and the subsequent invasion process itself. I will use an insertional genetic screen to identify proteins involved in invasion and its regulation. Furthermore, as a complementary approach, I will analyze the function of one protein known to be essential for invasion in detail. To accomplish this goal, I will use Toxoplasma gondii, an apicomplexan parasite that infects many warm-blooded animals, including humans. In addition to its importance as a pathogen in its own right, Toxoplasma has proven to be a highly tractable model for studying the mechanisms of cell invasion shared by apicomplexans; thus, my results will shed light on this critical process not only in Toxoplasma but also in the related human malaria parasites, Plasmodium spp.

• DFG-Verfahren: Forschungsstipendien
• Internationaler Bezug: USA
• Gastgeber: Professor John C. Boothroyd, Ph.D.