Abstract

Toxoplasma (toxoplasmosis) and Plasmodium (malaria) use unique secretory organelles for migration, cell invasion, manipulation of host cell functions, and cell egress. In particular, the apical secretory micronemes and rhoptries of apicomplexan parasites are essential for successful host infection. New findings reveal that the contents of these organelles, which are transported through the endoplasmic reticulum (ER) and Golgi, also require the parasite endosome-like system to access their respective organelles. In this review, we discuss recent findings that demonstrate that these parasites reduced their endosomal system and modified classical regulators of this pathway for the biogenesis of apical organelles.

Highlights

  • The phylum Apicomplexa is comprised of single-celled parasites of eminent clinical and economic importance including Plasmodium spp., the agents of malaria, and Toxoplasma gondii, the cause of toxoplasmosis

  • Powerful reverse genetic strategies in T. gondii have established that DrpB, TgSORTLR, Rab5A, Rab5C, and CHC1 act as key trafficking components at Golgi cisternae and proximal vesicles for the biogenesis of apical secretory organelles

  • Disrupting these proteins leads to the absence of host cell egress, gliding motility, cell invasion, and in vivo infection because of the crucial roles for apical secretory organelles in these events

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Summary

Introduction

The phylum Apicomplexa is comprised of single-celled parasites of eminent clinical and economic importance including Plasmodium spp., the agents of malaria, and Toxoplasma gondii, the cause of toxoplasmosis. Specialized regulated secretory organelles termed micronemes and rhoptries are crucial to cell invasion and intracellular survival of most apicomplexan parasites. Whereas dense granule formation likely occurs at the Golgi, the biogenesis of micronemes and rhoptries is distinguished by the involvement of the endosome-like system in T. gondii and possibly other apicomplexans.

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