Malaria parasite manipulates erythrocyte membranes for intracellular adaptation : RNA-seq

ABSTRACT: The ability to respond to stressful host environments is crucial for the survival of intracellular pathogens, during which transporters play key roles in the nutrient scavenging, such as lipid uptake. Here we discover a conserved malarial gene that orchestrates the parasitic adaption in the terminally differentiated, phospholipid scarce erythrocytes. The expression level of this gene, here named CAP, is the intensively upregulated in the erythrocyte-infecting parasites than the reticulocyte-infecting counterparts. We show that CAP encodes a small protein exported onto the membrane of infected erythrocytes where it interacts with host CTL1, a choline and ethanolamine transporter, and upregulates biosynthesis of phosphatidylcholine and phosphatidylethanolamine, the major component of parasite membrane. Deletion of CAP causes Plasmodium to upturn reticulocyte invasion and sexual stage differentiation. This work presents a novel mechanism for intracellular parasite to import lipid precursors into parasitized cells by manipulating an endogenous host transporter.

ORGANISM(S): Plasmodium berghei

PROVIDER: GSE252704 | GEO | 2024/01/12

REPOSITORIES: GEO