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A more recent version of this article appeared on June 1, 2002
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Submitted on August 9, 2001
Revised on February 19, 2002
Accepted on February 22, 2002
1 Universität Stuttgart, Pfaffenwaldring 55, 70569 Stuttgart, Germany
2 Max-Delbrück-Centrum für Molekulare Medizin, Robert-Rössle-Str. 10, 13125 Berlin, Germany
* Corresponding author. E-mail address: dieter.wolf{at}po.uni-stuttgart.de.
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, no other specific organelle for ER degradation could be identified by electron microscopy studies. As 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 endoplasmic reticulum 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.
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