Journal
TRAFFIC
Volume 9, Issue 12, Pages 2279-2290Publisher
WILEY
DOI: 10.1111/j.1600-0854.2008.00820.x
Keywords
endocytosis; enveloped virus; ESCRTs; intra-endosomal transport; multivesicular body; Tsg101; vesicular stomatitis virus
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Funding
- National Science Foundation
- Telethon Foundation
- Fondation pour la Recherche Medicale
- Marie Curie Intra-European Programme
- L'Association pour la Recherche contre le Cancer (ARC)
- Roche Foundation
- EMBO
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Like other enveloped viruses, vesicular stomatitis virus infects cells through endosomes. There, the viral envelope undergoes fusion with endosomal membranes, thereby releasing the nucleocapsid into the cytoplasm and allowing infection to proceed. Previously, we reported that the viral envelope fuses preferentially with the membrane of vesicles present within multivesicular endosomes. Then, these intra-endosomal vesicles (containing nucleocapsids) are transported to late endosomes, where back-fusion with the endosome limiting membrane delivers the nucleocapsid into the cytoplasm. In this study, we show that the tumor susceptibility gene 101 (Tsg101) subunit of the endosomal sorting complexes required for transport (ESCRT)-I complex, which mediates receptor sorting into multivesicular endosomes, is dispensable for viral envelope fusion with endosomal membranes and viral RNA transport to late endosomes but is necessary for infection. Our data indicate that Tsg101, in contrast to the ESCRT-0 component Hrs, plays a direct role in nucleocapsid release from within multivesicular endosomes to the cytoplasm, presumably by controlling the back-fusion process. We conclude that Tsg101, through selective interactions with its partners including Hrs and Alix, may link receptor sorting and lysosome targeting to the back-fusion process involved in viral capsid release.
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