【摘 要】
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ER-derived COPⅡ coated vesicles are targeted to the Golgi.However, during cell stress these vesicles are diverted to the canonical macroautophagy pathway where
【机 构】
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Cellular&MolecularMedicineDepartment,UniversityofCalifornia,SanDiego,LaJollaCA92093
【出 处】
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The 7th International Symposium on Autophagy 2015(第七届自噬国际研讨会
论文部分内容阅读
ER-derived COPⅡ coated vesicles are targeted to the Golgi.However, during cell stress these vesicles are diverted to the canonical macroautophagy pathway where they become a membrane source for the autophagosome, a unique compartment that targets unwanted proteins for degradation.We have shown that when macroautophagy is induced the TRAPPⅢ complex, a conserved autophagy-specific guanine nucleotide exchange factor for the Rab GTPase Ypt1 (Rab1 in mammals), is recruited to the preautophagosomal structure (PAS) by Atg17.In parallel with this event, Atg9 vesicles move from the Golgi to the PAS to initiate autophagosome formation.We have speculated that activated Ypt1 recruits the Atg1 kinase to the PAS to tether Atg9 vesicles to COPⅡ vesicles.Consistent with this proposal, COPⅡ vesicles and the ER-Golgi fusion machinery are needed for macroautophagy.Current studies,which show that Ypt1/Rab1 regulates ER-Golgi traffic and macroautophagy by a common mechanism, will be discussed.
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