Sec16 influences transitional ER sites by regulating rather than organizing COPII.

TitleSec16 influences transitional ER sites by regulating rather than organizing COPII.
Publication TypeJournal Article
Year of Publication2013
AuthorsBharucha, N, Liu, Y, Papanikou, E, McMahon, C, Esaki, M, Jeffrey, PD, Hughson, FM, Glick, BS
JournalMol Biol Cell
Volume24
Issue21
Pagination3406-19
Date Published2013 Nov
ISSN1939-4586
KeywordsBinding Sites, COP-Coated Vesicles, Cytosol, Endoplasmic Reticulum, Fungal Proteins, Green Fluorescent Proteins, Immunoblotting, Microscopy, Fluorescence, Mutation, Pichia, Protein Binding, Protein Transport, Two-Hybrid System Techniques
Abstract

<p>During the budding of coat protein complex II (COPII) vesicles from transitional endoplasmic reticulum (tER) sites, Sec16 has been proposed to play two distinct roles: negatively regulating COPII turnover and organizing COPII assembly at tER sites. We tested these ideas using the yeast Pichia pastoris. Redistribution of Sec16 to the cytosol accelerates tER dynamics, supporting a negative regulatory role for Sec16. To evaluate a possible COPII organization role, we dissected the functional regions of Sec16. The central conserved domain, which had been implicated in coordinating COPII assembly, is actually dispensable for normal tER structure. An upstream conserved region (UCR) localizes Sec16 to tER sites. The UCR binds COPII components, and removal of COPII from tER sites also removes Sec16, indicating that COPII recruits Sec16 rather than the other way around. We propose that Sec16 does not in fact organize COPII. Instead, regulation of COPII turnover can account for the influence of Sec16 on tER sites. </p>

DOI10.1091/mbc.E13-04-0185
Alternate JournalMol. Biol. Cell
PubMed ID24006484
PubMed Central IDPMC3814151
Grant ListR01 GM061156 / GM / NIGMS NIH HHS / United States
R01 GM071574 / GM / NIGMS NIH HHS / United States
T32 GM007388 / GM / NIGMS NIH HHS / United States