Protein interactions in the cytoskeleton of dysentery-causing entamoeba parasite provide clues for treatment
Amebiasis, infection with the parasitic eukaryote Entamoeba histolytica, affects around 50 million people worldwide, causing symptoms ranging from diarrhoea to liver abscesses. Entamoeba (pictured, in green) gobbles up red blood cells (in red), and microbes in its host’s gut, engulfing them by phagocytosis. This process requires its cytoskeleton, the network of protein filaments giving cells structure, to be very dynamic, changing shape as needed. Key to this flexibility is a protein named EhP3, one of a large family of eukaryotic proteins, the 14-3-3 proteins, which accumulates at the 'phagocytic cups', where the cell membrane curves to surround target cells. Downregulating EhP3 reduces the rate of phagocytosis, as EhP3 acts as a hub for organising cytoskeletal rearrangements, binding to many other proteins which in turn interact with actin fibres in the cytoskeleton. Understanding these protein interactions sheds light on a crucial process for this parasite, potentially uncovering targets for future treatments.
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