High levels of Fis1, a pro-fission mitochondrial protein, trigger autophagy.
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 Fis1 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 Fis1 mutants with different effects on organelle shape and function. In conclusion, fission associated with mitochondrial dysfunction stimulates an increase in autophagy.
Dulbecco-Telethon INStitute, Venetian INStitute of Molecular Medicine, Via Orus 2, 35129 Padova, Italy.
Ligia C
LC
Gomes
Luca
L
Scorrano
D000818:Animals; D001343:Autophagy; D002478:Cells, Cultured; D005347:Fibroblasts / Q000166:cytology / Q000502:physiology*; D006367:HeLa Cells; D006801:Humans; D008565:Membrane Proteins / Q000235:genetics* / Q000502:physiology*; D051379:Mice; D008928:Mitochondria / Q000502:physiology* / Q000648:ultrastructure; D024101:Mitochondrial Proteins / Q000235:genetics / Q000502:physiology*
C476525:FIS1 protein, human; D008565:Membrane Proteins; D024101:Mitochondrial Proteins