A 3D view of the host cell compartment in P. falciparum-infected erythrocytes.
The most deadly of the human malaria parasites, Plasmodium falciparum, invades the erythrocytes of its host and initiates a remarkable series of morphological rearrangements within the host cell cytoplasm. The mature erythrocyte is effectively a floating sack of haemoglobin with no endogenous protein synthesis or protein trafficking machinery. In order to colonise and remodel its extracellular space, the parasite generates a series of novel structures that are involved in the export of virulence factors to the surface of the host cell. These include extensions of the parasite's vacuolar membrane, known as the tubulovesicular network, and structures referred to as Maurer's clefts. Maurer's clefts are convoluted collections of distorted discs that are tethered to the red blood cell membrane by structures with stalk-like profiles. Recently electron tomography has enabled visualisation--in three dimensions and at unprecedented resolution--the complexity of the membrane systems within the infected RBC cytoplasm.
Tilley
L
L
Department of Biochemistry and Centre of Excellence for Coherent X-ray Science, La Trobe University, Melbourne, Victoria 3086, Australia. l.tilley@latrobe.edu.au
Hanssen
E
E
D000818:Animals; D004912:Erythrocytes / Q000469:parasitology* / Q000648:ultrastructure*; D016778:Malaria, Falciparum / Q000473:pathology*; D008854:Microscopy, Electron / Q000379:methods; D010963:Plasmodium falciparum / Q000648:ultrastructure*; D021381:Protein Transport; D015800:Protozoan Proteins / Q000032:analysis / Q000378:metabolism
D015800:Protozoan Proteins; C085731:erythrocyte membrane protein 1, Plasmodium falciparum