DiscussionPlasmodium parasites are the causative agent of malaria and are transmitted by Anopheles mosquitoes. Before the clinically relevant blood stage, the parasites infect hepatocytes where they reside in a special compartment called parasitophorous vacuole (PV). We use the rodent malaria model parasite Plasmodium berghei to investigate the liver stage. A host cell autophagy-related process plays an important role in the control of liver stage Plasmodium parasites. Previously, we have shown that autophagy markers, like LC3, localise to the PV membrane (PVM) in early liver stages. It has been found that viable parasites can exclude LC3 from the PVM by membrane shedding. To prove membrane shedding by biophysical means, we expressed parasite and host cell PVM proteins tagged with photo-convertible fluorescent proteins and analyse their localization before and after photo-conversion. Intravital imaging of mice infected with fluorescent P. berghei parasites support these in vitro obtained data.