Abstract
During the asexual intraerythrocytic stage, the malaria parasite Plasmodium falciparum must traffic newly-synthesized proteins to a broad array of destinations within and beyond the parasite's plasma membrane. In this study, we have localized two well-conserved protein components of eukaryotic endosomes, the retromer complex and the small GTPase Rab7, to define a previously-undescribed endosomal compartment in P. falciparum. Retromer and Rab7 co-localized to a small number of punctate structures within parasites. These structures, which we refer to as endosomes, lie in close proximity to the Golgi apparatus and, like the Golgi apparatus, are inherited by daughter merozoites. However, the endosome is clearly distinct from the Golgi apparatus as neither retromer nor Rab7 redistributed to the endoplasmic reticulum upon brefeldin A treatment. Nascent rhoptries (specialized secretory organelles required for invasion) developed adjacent to endosomes, an observation that suggests a role for the endosome in rhoptry biogenesis. A P. falciparum homolog of the sortilin family of protein sorting receptors (PfSortilin) was localized to the Golgi apparatus. Together, these results elaborate a putative Golgi-to-endosome protein sorting pathway in asexual blood stage parasites and suggest that one role of retromer is to mediate the retrograde transport of PfSortilin from the endosome to the Golgi apparatus.
Highlights
The human malaria parasite Plasmodium falciparum is responsible for approximately one million deaths annually [1]
In addition to the cargo-selective complex, a second component of the retromer complex in mammals and yeast is a PX-BAR sorting nexin dimer, which binds to PI3P through the Phox (PX) domains and induces or stabilizes membrane curvature with the BAR domains [22,33,34,35]
When we restricted the search to the PX domains, we found two PX domain-containing proteins in the P. falciparum genome but neither appeared to be followed by a BAR domain
Summary
The human malaria parasite Plasmodium falciparum is responsible for approximately one million deaths annually [1]. The parasite undergoes a ,48 hour replication cycle, generating 8–26 daughter merozoites that egress from the spent host cell and invade fresh erythrocytes [2] During this cycle, the parasite must replicate its heritable organelles (the nucleus, endoplasmic reticulum, Golgi apparatus, mitochondrion and apicoplast) and generate others de novo. The parasite must replicate its heritable organelles (the nucleus, endoplasmic reticulum, Golgi apparatus, mitochondrion and apicoplast) and generate others de novo Of the latter group, the food vacuole, rhoptries, micronemes, and dense granules are the best characterized [3,4] but other compartments (exonemes and mononemes) have been reported [5,6]. Micronemes and dense granules are specialized, apically oriented secretory organelles that discharge their contents during and shortly after host cell invasion
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