Scientific Reports (Feb 2021)

Syntenin-knock out reduces exosome turnover and viral transduction

  • 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

DOI
https://doi.org/10.1038/s41598-021-81697-4
Journal volume & issue
Vol. 11, no. 1
pp. 1 – 12

Abstract

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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.