Abstract
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 dyelabeled 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.
Original language | English (US) |
---|---|
Article number | jcs235507 |
Journal | Journal of cell science |
Volume | 132 |
Issue number | 16 |
DOIs | |
State | Published - Aug 2019 |
Keywords
- Cell adhesion
- Cell communication
- Cytoplasm transfer
- Measles virsus
- Nectin
- Neuronal entry
- Transendocytosis
- Virus receptor
ASJC Scopus subject areas
- Cell Biology