We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
Dissecting the involvement of LC3B and GATE-16 in p62 recruitment into autophagosomes.
- Authors
Shvets, Elena; Abada, Adi; Weidberg, Hilla; Elazar, Zvulun
- Abstract
Autophagy is a major intracellular trafficking pathway that delivers proteins and organelles from the cytoplasm into lysosomes for consequential degradation and recycling. Mammalian Atg8s are key autophagic factors that undergo a unique ubiquitin-like conjugation to the lipid phase of the autophagosomal membrane. In addition to their activity in autophagosome formation, several Atg8s directly bind p62/SQSTM1. Here we show that LC3 and GATE-16 differ in their mode of p62 binding. While the soluble form of both LC3 and GATE-16 bind p62, only the lipidated form of LC3 is directly involved in p62 recruitment into autophagosomes. Moreover, by utilizing chimeras of LC3 and GATE-16 where their N-terminus was swapped, we determined the regions responsible for this differential binding. Accordingly, we found that the chimera of GATE-16 containing the LC3 N-terminal region acts similarly to wild-type LC3 in recruiting p62 into autophagosomes. We therefore propose that LC3 is responsible for the final stages of p62 incorporation into autophagosomes, a process selectively mediated by its N-terminus.
- Publication
Autophagy, 2011, Vol 7, Issue 7, p683
- ISSN
1554-8635
- Publication type
Journal Article
- DOI
10.4161/auto.7.7.15279