The twists and turns of Maurer's cleft trafficking in P. falciparum-infected erythrocytes.
The malaria parasite, Plasmodium falciparum, invades the red blood cells (RBCs) of its human host and initiates a series of morphological rearrangements within the host cell cytoplasm. The mature RBC has no endogenous trafficking machinery; therefore, the parasite generates novel structures to mediate protein transport. These include compartments called the Maurer's clefts (MC), which play an important role in the trafficking of parasite proteins to the surface of the host cell. Recent electron tomography studies have revealed MC as convoluted flotillas of flattened discs that are tethered to the RBC membrane, prompting speculation that the MC could, in one respect, represent an extracellular equivalent of the Golgi apparatus. Visualization of both resident and cargo proteins has helped decipher the signals and routes for trafficking of parasite proteins to the MC and beyond.
Tilley
Leann
L
Department of Biochemistry, La Trobe University, Melbourne, Victoria 3086, Australia.
Sougrat
Rachid
R
Lithgow
Trevor
T
Hanssen
Eric
E
D000818:Animals; D022083:Cytoplasmic Structures / Q000000981:diagnostic imaging / Q000378:metabolism* / Q000469:parasitology; D004912:Erythrocytes / Q000378:metabolism* / Q000469:parasitology / Q000648:ultrastructure; D006801:Humans; D008854:Microscopy, Electron; D008954:Models, Biological; D010963:Plasmodium falciparum / Q000502:physiology*; D021382:Protein Sorting Signals / Q000502:physiology; D021381:Protein Transport / Q000502:physiology; D014463:Ultrasonography
D021382:Protein Sorting Signals