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Sec16 influences transitional ER sites by regulating rather than organizing COPII
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 pastor...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The American Society for Cell Biology
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3814151/ https://www.ncbi.nlm.nih.gov/pubmed/24006484 http://dx.doi.org/10.1091/mbc.E13-04-0185 |
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author | Bharucha, Nike Liu, Yang Papanikou, Effrosyni McMahon, Conor Esaki, Masatoshi Jeffrey, Philip D. Hughson, Frederick M. Glick, Benjamin S. |
author_facet | Bharucha, Nike Liu, Yang Papanikou, Effrosyni McMahon, Conor Esaki, Masatoshi Jeffrey, Philip D. Hughson, Frederick M. Glick, Benjamin S. |
author_sort | Bharucha, Nike |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-3814151 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | The American Society for Cell Biology |
record_format | MEDLINE/PubMed |
spelling | pubmed-38141512014-01-16 Sec16 influences transitional ER sites by regulating rather than organizing COPII Bharucha, Nike Liu, Yang Papanikou, Effrosyni McMahon, Conor Esaki, Masatoshi Jeffrey, Philip D. Hughson, Frederick M. Glick, Benjamin S. Mol Biol Cell Articles 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. The American Society for Cell Biology 2013-11-01 /pmc/articles/PMC3814151/ /pubmed/24006484 http://dx.doi.org/10.1091/mbc.E13-04-0185 Text en © 2013 Bharucha et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0). “ASCB®,” “The American Society for Cell Biology®,” and “Molecular Biology of the Cell®” are registered trademarks of The American Society of Cell Biology. |
spellingShingle | Articles Bharucha, Nike Liu, Yang Papanikou, Effrosyni McMahon, Conor Esaki, Masatoshi Jeffrey, Philip D. Hughson, Frederick M. Glick, Benjamin S. Sec16 influences transitional ER sites by regulating rather than organizing COPII |
title | Sec16 influences transitional ER sites by regulating rather than organizing COPII |
title_full | Sec16 influences transitional ER sites by regulating rather than organizing COPII |
title_fullStr | Sec16 influences transitional ER sites by regulating rather than organizing COPII |
title_full_unstemmed | Sec16 influences transitional ER sites by regulating rather than organizing COPII |
title_short | Sec16 influences transitional ER sites by regulating rather than organizing COPII |
title_sort | sec16 influences transitional er sites by regulating rather than organizing copii |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3814151/ https://www.ncbi.nlm.nih.gov/pubmed/24006484 http://dx.doi.org/10.1091/mbc.E13-04-0185 |
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