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

Biochim Biophys Acta. Jul-Aug 2008;1777(7-8):860-6. doi: 10.1016/j.bbabio.2008.05.442. Epub 2008 May 26.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Autophagy
  • Cells, Cultured
  • Fibroblasts / cytology
  • Fibroblasts / physiology*
  • HeLa Cells
  • Humans
  • Membrane Proteins / genetics*
  • Membrane Proteins / physiology*
  • Mice
  • Mitochondria / physiology*
  • Mitochondria / ultrastructure
  • Mitochondrial Proteins / genetics
  • Mitochondrial Proteins / physiology*

Substances

  • FIS1 protein, human
  • Membrane Proteins
  • Mitochondrial Proteins