Yorimitsu T and Sato K (2012) Insights into structural and regulatory roles of Sec16 in COPII vesicle formation at ER exit sites. Mol Biol Cell 23(15):2930-42
Abstract: COPII-coated buds are formed at endoplasmic reticulum exit sites (ERES) to mediate ER-to-Golgi transport. Sec16 is an essential factor in ERES formation, as well as in COPII-mediated traffic in vivo. Sec16 interacts with multiple COPII proteins, although the functional significance of these interactions remains unknown. Here we present evidence that full-length Sec16 plays an important role in regulating Sar1 GTPase activity at the late steps of COPII vesicle formation. We show that Sec16 interacts with Sec23 and Sar1 through its C-terminal conserved region and hinders the ability of Sec31 to stimulate Sec23 GAP activity toward Sar1. We also find that purified Sec16 alone can self-assemble into homo-oligomeric complexes on a planar lipid membrane. These features ensure prolonged COPII coat association within a preformed Sec16 cluster, which may lead to the formation of ERES. Our results indicate a mechanistic relationship between COPII coat assembly and ERES formation.
|Status: Published||Type: Journal Article | Research Support, Non-U.S. Gov't||PubMed ID: 22675024|
Topics addressed in this paper
Number of different genes curated to this paper: 4
- To go to the Locus page for a gene, click on the gene name.