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Here, we show that cells expressing the adherens junction protein nectin-1 capture nectin-4-containing membranes from the surface of adjacent cells in a trans-endocytosis process. We find that internalized nectin-1-nectin-4 complexes follow the endocytic pathway. The nectin-1 cytoplasmic tail controls transfer: its deletion prevents trans-endocytosis, while its exchange with the nectin-4 tail reverses transfer direction. Nectin-1-expressing cells acquire dye-labeled cytoplasmic proteins synchronously with nectin-4, a process most active during cell adhesion. Some cytoplasmic cargo remains functional after transfer, as demonstrated with encapsidated genomes of measles virus (MeV). This virus uses nectin-4, but not nectin-1, as a receptor. Epithelial cells expressing nectin-4, but not those expressing another MeV receptor in its place, can transfer infection to nectin-1-expressing primary neurons. Thus, this newly discovered process can move cytoplasmic cargo, including infectious material, from epithelial cells to neurons. We name the process nectin-elicited cytoplasm transfer (NECT). NECT-related trans-endocytosis processes may be exploited by pathogens to extend tropism. This article has an associated First Person interview with the first author of the paper. © 2019. Published by The Company of Biologists Ltd.

Citation

Alex R Generous, Oliver J Harrison, Regina B Troyanovsky, Mathieu Mateo, Chanakha K Navaratnarajah, Ryan C Donohue, Christian K Pfaller, Olga Alekhina, Alina P Sergeeva, Indrajyoti Indra, Theresa Thornburg, Irina Kochetkova, Daniel D Billadeau, Matthew P Taylor, Sergey M Troyanovsky, Barry Honig, Lawrence Shapiro, Roberto Cattaneo. Trans-endocytosis elicited by nectins transfers cytoplasmic cargo, including infectious material, between cells. Journal of cell science. 2019 Aug 23;132(16)

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PMID: 31331966

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