Abstract
Clathrin-coated vesicles (CCVs) are formed at the plasma membrane and act as vectors for endocytosis. They also assemble at the trans-Golgi network (TGN), but their exact function at this organelle is unclear. Recent studies have examined the effects on vacuolar and secretory protein transport of knockout mutations of the adaptor protein 1 (AP1) μ-adaptin subunit AP1M, but these investigations do not clarify the situation. These mutations lead to the abrogation of multiple trafficking pathways at the TGN and cannot be used as evidence in favour of CCVs being agents for receptor-mediated export of vacuolar proteins out of the TGN. This transport process could just as easily occur through the maturation of the TGN into intermediate compartments that subsequently fuse with the vacuole.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
