Abstract
The protozoan parasite Entamoeba histolytica is the aetiologic agent of amoebiasis, an endemic infection in developing countries with considerable morbidity and mortality. Recently, trogocytosis has been recognized as the key step in amoebic cytolysis and invasion, a paradigm shift in understanding pathogenicity of this organism. Here we report that AGC family kinase 1 is specifically involved in trogocytosis of live human cells and does not participate in phagocytosis of dead cells. Live imaging reveals localization of this kinase in the long and thin tunnels formed during trogocytosis but not in the trogosomes (endosomes formed after trogocytosis). Silencing of the specific gene leads to a defect in CHO cell destruction and trogocytosis while other endocytic processes remain unaffected. The results suggest that the trogocytic pathway is likely to be different from phagocytosis though many of the steps and molecules involved may be common.
Highlights
The protozoan parasite Entamoeba histolytica is the aetiologic agent of amoebiasis, an endemic infection in developing countries with considerable morbidity and mortality
Host-cell destruction is thought to be through the process of trogocytosis, that is, ingestion of several fragments of live cells in multiple steps leading to elevation of Ca2+ in cytosol, loss of plasma membrane integrity and eventually death of the cells9
Live cells undergo trogocytosis by E. histolytica, whereas dead cells are taken up by phagocytosis9. It appears that amoebic trogocytosis overlaps with the signalling pathway of erythrophagocytosis involving EhC2PK and PI3K, suggesting that the same pathway is at least partially used for different endocytic processes
Summary
The protozoan parasite Entamoeba histolytica is the aetiologic agent of amoebiasis, an endemic infection in developing countries with considerable morbidity and mortality. Live cells undergo trogocytosis by E. histolytica, whereas dead cells are taken up by phagocytosis9 It appears that amoebic trogocytosis overlaps with the signalling pathway of erythrophagocytosis involving EhC2PK and PI3K, suggesting that the same pathway is at least partially used for different endocytic processes. It is still not clear what makes only live cells undergo trogocytosis. Myosin1B and EhCaBP3 have been implicated in phagosome fusion and separation from plasma membrane14, 15 Though some of these molecules are involved in fluid-phase pinocytosis and trogocytosis, it is not clear how these three processes (phagocytosis, pinocytosis and trogocytosis) differ from each other at the molecular level. Vav and Rac proteins are phosphorylated in a PtdIns[3,4,5]P3-dependent manner, resulting in activation of actin machinery through Wiskott-Aldrich syndrome protein and Arp2/3 pathway
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