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PMID: 17040485 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Review

Endoplasmic reticulum and Golgi complex: Contributions to, and turnover by, autophagy.

Traffic (Copenhagen, Denmark) ·Vol. 7 ·No. 12 ·2006-12-00 ·Pages 1590-5

Mijaljica D, Prescott M, Devenish RJ

Abstract

The degradation of cytoplasmic contents, especially organelles [mitochondria, peroxisomes, endoplasmic reticulum (ER), Golgi complex (GC)], cannot be accomplished solely by the cytosolic degradation machinery, of which the most prominent component is the proteasome. However, it is possible that such organelles (or portions thereof) can be degraded by the cell's autophagic machinery. In this manner, organelles can be either specifically or non-specifically targeted to the vacuole/lysosome for degradation. These processes can be triggered in response to different environmental cues. Here, we focus on two particular organelles, the ER and the GC, and their relationship with the autophagic process. Firstly, we briefly consider how these two organelles contribute to the synthesis and delivery of hydrolytic enzymes involved in autophagy as well as how they may potentially contribute to their own degradation by addressing the origin of the autophagic membrane. Secondly, we summarize the evidence for the turnover of these two organelles by autophagic processes in different organisms.

MeSH Terms
Animals Autophagy Endoplasmic Reticulum/metabolism Golgi Apparatus/metabolism Intracellular Membranes/metabolism Organelles/metabolism Protein Transport
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Mijaljica Dalibor
Department of Biochemistry and Molecular Biology, and the ARC Centre of Excellence in Structural and Functional Microbial Genomics, Monash University, Melbourne, Vic. 3800, Australia.
Prescott Mark
Devenish Rodney J
Article Info
Journal
Traffic (Copenhagen, Denmark)
Abbr.
Traffic
ISSN
1398-9219
Published
2006-12-00
Epub
2006-00-16
Pages
1590-5
Language
English
Region
England
NLM ID
100939340
Subset
IM
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