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

被引:50
作者
Mijaljica, Dalibor
Prescott, Mark
Devenish, Rodney J. [1 ]
机构
[1] Monash Univ, Dept Biochem & Mol Biol, Melbourne, Vic 3800, Australia
[2] ARC Ctr Excellence Struct & Funct Microbial Genom, Melbourne, Vic 3800, Australia
关键词
autophagosome; autophagy; degradation; endomembrane; endoplasmic reticulum; Golgi complex; lysosome; organelles; vacuole; vesicle;
D O I
10.1111/j.1600-0854.2006.00495.x
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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.
引用
收藏
页码:1590 / 1595
页数:6
相关论文
共 51 条
  • [11] Maturation of autophagic vacuoles in mammalian cells
    Eskelinen, Eeva-Liisa
    [J]. AUTOPHAGY, 2005, 1 (01) : 1 - 10
  • [12] The dynamic ER: experimental approaches and current questions
    Federovitch, CM
    Ron, D
    Hampton, RY
    [J]. CURRENT OPINION IN CELL BIOLOGY, 2005, 17 (04) : 409 - 414
  • [13] ELIMINATION OF EXCESS SMOOTH ENDOPLASMIC-RETICULUM AFTER PHENOBARBITAL ADMINISTRATION
    FELDMAN, D
    SWARM, RL
    BECKER, J
    [J]. JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY, 1980, 28 (09) : 997 - 1006
  • [14] Fengsrud M, 2004, AUTOPHAGY, P11
  • [15] Starvation triggers the delivery of the endoplasmic reticulum to the vacuole via autophagy in yeast
    Hamasaki, M
    Noda, T
    Baba, M
    Ohsumi, Y
    [J]. TRAFFIC, 2005, 6 (01) : 56 - 65
  • [16] Ubiquitination of a yeast plasma membrane receptor signals its ligand-stimulated endocytosis
    Hicke, L
    Riezman, H
    [J]. CELL, 1996, 84 (02) : 277 - 287
  • [17] Autophagosome requires specific early Sec proteins for its formation and NSF/SNARE for vacuolar fusion
    Ishihara, N
    Hamasaki, M
    Yokota, S
    Suzuki, K
    Kamada, Y
    Kihara, A
    Yoshimori, T
    Noda, T
    Ohsumi, Y
    [J]. MOLECULAR BIOLOGY OF THE CELL, 2001, 12 (11) : 3690 - 3702
  • [18] Excess peroxisomes are degraded by autophagic machinery in mammals
    Iwata, J
    Ezaki, J
    Komatsu, M
    Yokota, S
    Ueno, T
    Tanida, I
    Chiba, T
    Tanaka, K
    Kominami, E
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2006, 281 (07) : 4035 - 4041
  • [19] Autophagy: A forty-year search for a missing membrane source
    Juhasz, G
    Neufeld, TP
    [J]. PLOS BIOLOGY, 2006, 4 (02) : 161 - 164
  • [20] Intracellular inclusions containing mutant α1-antitrypsin Z are propagated in the absence of autophagic activity
    Kamimoto, T
    Shoji, S
    Hidvegi, T
    Mizushima, N
    Umebayashi, K
    Perlmutter, DH
    Yoshimori, T
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2006, 281 (07) : 4467 - 4476