Molecular Biology of the Cell track citations

Home Help [Feedback] [For Subscribers] [Archive] [Search] --
QUICK SEARCH:   [advanced]


     

MBC in Press, published online ahead of print February 1, 2006
Mol. Biol. Cell 10.1091/mbc.E05-02-0100

A more recent version of this article appeared on April 1, 2006
This Article
Right arrow Full Text (PDF)
Right arrow Supplemental Material
Right arrow All Versions of this Article:
E05-02-0100v1
17/4/1593    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ridsdale, A.
Right arrow Articles by Zha, X.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ridsdale, A.
Right arrow Articles by Zha, X.

Submitted on February 7, 2005
Revised on January 19, 2006
Accepted on January 20, 2006

Cholesterol Is Required for Efficient ER-to-Golgi Transport of Secretory Membrane Proteins

Andrew Ridsdale,* Maxime Denis,* Pierre-Yves Gougeon,* Johnny K. Ngsee,* John F. Presley,{dagger} and Xiaohui Zha*

*Ottawa Health Research Institute and University of Ottawa, Ottawa, Ontario K1Y 4E9, Canada; and {dagger}Department of Anatomy and Cell Biology, McGill University, Montreal, Quebec H3A 2B2, Canada

Monitoring Editor: Sean Munro

Although cholesterol is synthesized in the ER, compared with other cellular membranes, ER membrane has low cholesterol (3-6%). Most of the molecular machinery that regulates cellular cholesterol homeostasis also resides in the ER. Little is known about how cholesterol itself affects the ER membrane. Here we demonstrate that acute cholesterol depletion in ER membranes impairs ER to Golgi transport of secretory membrane proteins. Cholesterol depletion is achieved by a brief inhibition of cholesterol synthesis with statins in cells grown in cholesterol depleted medium. We provide evidence that secretory membrane proteins, vesicular stomatitis virus glycoprotein (VSVG) and scavenger receptor A (SRA), failed to be efficiently transported from the ER upon cholesterol depletion. Fluorescence photobleaching recovery experiments indicated that cholesterol depletion by statins leads to a severe loss of lateral mobility on the ER membrane of these transmembrane proteins, but not loss of mobility of proteins in the ER lumen. This impaired lateral mobility is correlated with impaired ER to Golgi transport. These results provide evidence for the first time that cholesterol is required in the ER membrane to maintain mobility of membrane proteins and thus protein secretion.

Address correspondence to: Xiaohui Zha (xzha{at}ohri.ca)




This article has been cited by other articles:


Home page
 J. Cell Sci.Home page
A. Dukhovny, A. Papadopulos, and K. Hirschberg
Quantitative live-cell analysis of microtubule-uncoupled cargo-protein sorting in the ER
J. Cell Sci., March 15, 2008; 121(6): 865 - 876.
[Abstract] [Full Text] [PDF]


Home Help [Feedback] [For Subscribers] [Archive] [Search] --
Copyright © 2006 by The American Society for Cell Biology. Terms of copyright protection, warranties, and disclaimers.