Research Interests

Lipids transport is mediated by the Plasmodium falciparum Niemann-Pick C1 related protein (PfNCR1) in regions of close apposition of PVM with the parasite plasma membrane (PPM). The regions in which lipid transport is facilitated complement regions where proteins are exported and small hydrophilic molecules cross the PVM by EXP2, have been thus far completely unexplored. Investigating the mechanisms that form the close membrane apposition and mediate transport of lipids are essential in completing our understanding of how the parasite interacts with its environment.

Membrane remodeling is an early, critical event of the parasite establishing residence in its host-cell. Pinching-off the parasitophorous vacuole, the creation of the parasite-generated host trafficking organelles (Maurer’s clefts) requires membrane scission events. Membrane trafficking machinery is not evident from homology search. Later the parasite endocytoses host-cytosol for its amino acids and to create space to grow. It is unknown how the parasite coordinates PVM and PPM for uptake and how double membrane scission is mediated.

Both membrane remodeling mechanisms are essential for parasite survival and fundamental for communication of the parasite with its environment.

The malaria parasite evolved an intricate ensemble of mechanisms to invade and take over red blood cells. Reconstituting the mechanisms the parasite uses to take over red blood cells helps define the minimal essential machinery we need to interfere with and stop the parasite from establishing infection, but also naturally leads the way to re-engineered red blood cells as tool that could deliver medicines.

Manipulating invasion mechanisms offers the opportunity to transform knowledge about the parasite into a tool for human health, translating the unique cell biology of the parasite to a treatment.