Scientific article

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

Published inBiochimica et biophysica acta, vol. 1777, no. 7-8, p. 860-866
Publication date2008

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.

  • Animals
  • Autophagy
  • Cells, Cultured
  • Fibroblasts/cytology/*physiology
  • HeLa Cells
  • Humans
  • Membrane Proteins/*genetics/*physiology
  • Mice
  • Mitochondria/*physiology/ultrastructure
  • Mitochondrial Proteins/genetics/*physiology
Citation (ISO format)
GOMES, Ligia C., SCORRANO, Luca. High levels of Fis1, a pro-fission mitochondrial protein, trigger autophagy. In: Biochimica et biophysica acta, 2008, vol. 1777, n° 7-8, p. 860–866. doi: 10.1016/j.bbabio.2008.05.442
Updates (1)
ISSN of the journal0006-3002

Technical informations

Creation03/27/2012 9:23:13 AM
First validation03/27/2012 9:23:13 AM
Update time03/14/2023 5:20:06 PM
Status update03/14/2023 5:20:06 PM
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