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ER-Golgi traffic is a prerequisite for efficient ER degradation

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Item Type:Article
Title:ER-Golgi traffic is a prerequisite for efficient ER degradation
Creators Name:Taxis, C. and Vogel, F. and Wolf, D.H.
Abstract:Protein quality control is an essential function of the endoplasmic reticulum. Misfolded proteins unable to acquire their native conformation are retained in the endoplasmic reticulum, retro-translocated back into the cytosol, and degraded via the ubiquitin-proteasome system. We show that efficient degradation of soluble malfolded proteins in yeast requires a fully competent early secretory pathway. Mutations in proteins essential for ER-Golgi protein traffic severely inhibit ER degradation of the model substrate CPY*. We found ER localization of CPY* in WT cells, but no other specific organelle for ER degradation could be identified by electron microscopy studies. Because CPY* is degraded in COPI coat mutants, only a minor fraction of CPY* or of a proteinaceous factor required for degradation seems to enter the recycling pathway between ER and Golgi. Therefore, we propose that the disorganized structure of the ER and/or the mislocalization of Kar2p, observed in early secretory mutants, is responsible for the reduction in CPY* degradation. Further, we observed that mutations in proteins directly involved in degradation of malfolded proteins (Der1p, Der3/Hrd1p, and Hrd3p) lead to morphological changes of the endoplasmic reticulum and the Golgi, escape of CPY* into the secretory pathway and a slower maturation rate of wild-type CPY.
Keywords:Cycloheximide, Endoplasmic Reticulum, Genotype, Golgi Apparatus, Kinetics, Plasmids, Protein Folding, Saccharomyces Cerevisiae Proteins, Second Messenger Systems
Source:Molecular Biology of the Cell
Publisher:American Society for Cell Biology
Page Range:1806-1818
Date:1 June 2002
Additional Information:Copyright (c) 2002 by The American Society for Cell Biology
Official Publication:https://doi.org/10.1091/mbc.01-08-0399
PubMed:View item in PubMed

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