Syntenin-knock out reduces exosome turnover and viral transduction

Author:

Kashyap Rudra,Balzano Marielle,Lechat Benoit,Lambaerts Kathleen,Egea-Jimenez Antonio LuisORCID,Lembo Frédérique,Fares Joanna,Meeussen Sofie,Kügler Sebastian,Roebroek Anton,David Guido,Zimmermann Pascale

Abstract

AbstractExosomal transfers represent an important mode of intercellular communication. Syntenin is a small scaffold protein that, when binding ALIX, can direct endocytosed syndecans and syndecan cargo to budding endosomal membranes, supporting the formation of intraluminal vesicles that compose the source of a major class of exosomes. Syntenin, however, can also support the recycling of these same components to the cell surface. Here, by studying mice and cells with syntenin-knock out, we identify syntenin as part of dedicated machinery that integrates both the production and the uptake of secreted vesicles, supporting viral/exosomal exchanges. This study significantly extends the emerging role of heparan sulfate proteoglycans and syntenin as key components for macromolecular cargo internalization into cells.

Publisher

Springer Science and Business Media LLC

Subject

Multidisciplinary

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