Syntenin-knock out reduces exosome turnover and viral transduction

Abstract Exosomal 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...

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Autores principales: Rudra Kashyap, Marielle Balzano, Benoit Lechat, Kathleen Lambaerts, Antonio Luis Egea-Jimenez, Frédérique Lembo, Joanna Fares, Sofie Meeussen, Sebastian Kügler, Anton Roebroek, Guido David, Pascale Zimmermann
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2021
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Acceso en línea:https://doaj.org/article/5818175db7fd4b9fba6c41d314e2d576
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Sumario:Abstract Exosomal 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.