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Apicomplexan parasites invade host cells and immediately initiate cell division. The extracellular parasite discharges transmembrane proteins onto its surface to mediate motility and invasion. These are shed by intramembrane cleavage, a process associated with invasion but otherwise poorly understood. Functional analysis of Toxoplasma rhomboid 4, a surface intramembrane protease, by conditional overexpression of a catalytically inactive form produced a profound block in replication. This was completely rescued by expression of the cleaved cytoplasmic tail of Toxoplasma or Plasmodium apical membrane antigen 1 (AMA1). These results reveal an unexpected function for AMA1 in parasite replication and suggest that invasion proteins help to promote parasite switch from an invasive to a replicative mode.

Original publication

DOI

10.1126/science.1199284

Type

Journal article

Journal

Science

Publication Date

28/01/2011

Volume

331

Pages

473 - 477

Keywords

Antigens, Protozoan, Cell Cycle, Cell Division, Cell Membrane, Cells, Cultured, Fibroblasts, Humans, Membrane Proteins, Movement, Mutant Proteins, Plasmodium falciparum, Protozoan Proteins, Serine Proteases, Signal Transduction, Toxoplasma