High levels of Fis1, a pro-fission mitochondrial protein, trigger autophagy

被引:200
作者
Gomes, Ligia C. [1 ]
Scorrano, Luca [1 ]
机构
[1] Venetian Inst Mol Med, Dulbecco Telethon Inst, I-35129 Padua, Italy
来源
BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS | 2008年 / 1777卷 / 7-8期
关键词
mitochondria; fission; Fis1; autophagy;
D O I
10.1016/j.bbabio.2008.05.442
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Damaged mitochondria can be eliminated in a process of organelle autophagy, termed mitophagy. In most cells, the organization of mitochondria in a network could interfere with the selective elimination of damaged ones. In principle, fission of this network should precede mitophagy; but it is unclear whether it is per se a trigger of autophagy. The pro-fission mitochondrial protein Fisl induced mitochondrial fragmentation and enhanced the formation of autophagosomes which could enclose mitochondria. These changes correlated with mitochondrial dysfunction rather than with fragmentation, as substantiated by Fisl mutants with different effects on organelle shape and function. In conclusion, fission associated with mitochondrial dysfunction stimulates an increase in autophagy. (c) 2008 Elsevier B.V. All rights reserved.
引用
收藏
页码:860 / 866
页数:7
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