Abstract
Extracellular vesicles (EV) secreted by pathogens function in a variety of biological processes. Here, we demonstrate that in the protozoan parasite Trypanosoma brucei, exosome secretion is induced by stress that affects trans-splicing. Following perturbations in biogenesis of spliced leader RNA, which donates its spliced leader (SL) exon to all mRNAs, or after heat-shock, the SL RNA is exported to the cytoplasm and forms distinct granules, which are then secreted by exosomes. The exosomes are formed in multivesicular bodies (MVB) utilizing the endosomal sorting complexes required for transport (ESCRT), through a mechanism similar to microRNA secretion in mammalian cells. Silencing of the ESCRT factor, Vps36, compromised exosome secretion but not the secretion of vesicles derived from nanotubes. The exosomes enter recipient trypanosome cells. Time-lapse microscopy demonstrated that cells secreting exosomes or purified intact exosomes affect social motility (SoMo). This study demonstrates that exosomes are delivered to trypanosome cells and can change their migration. Exosomes are used to transmit stress signals for communication between parasites.
Highlights
The African trypanosomes are protozoan parasites that cause a fatal infection in both humans and livestock, and constitute a major economic burden
We demonstrate that exosomes are secreted from Trypanosoma brucei parasites when trans-splicing is inhibited
These exosomes contain, among many other constituents, a type of RNA known as spliced leader RNA (SL RNA), which is essential in these parasites for formation of all mature mRNA
Summary
The African trypanosomes are protozoan parasites that cause a fatal infection in both humans and livestock, and constitute a major economic burden. These parasites cycle between two hosts, mammals and flies. The active migration of the parasites within the insect host is essential for moving to the midgut against active forces of the digestive flow as the parasites enter the fly, but is essential for migration from the midgut via the proventriculus to the salivary glands This migration constitute a major bottleneck in the parasite life cycle [3]
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