Editor: Claude Gaillardin
Mitophagy in yeast: actors and physiological roles
Article first published online: 5 NOV 2010
© 2010 Federation of European Microbiological Societies. Published by Blackwell Publishing Ltd. All rights reserved
FEMS Yeast Research
Special Issue: Yeasts as a Model for Human Diseases
Volume 10, Issue 8, pages 1023–1034, December 2010
How to Cite
Bhatia-Kiššová, I. and Camougrand, N. (2010), Mitophagy in yeast: actors and physiological roles. FEMS Yeast Research, 10: 1023–1034. doi: 10.1111/j.1567-1364.2010.00659.x
- Issue published online: 5 NOV 2010
- Article first published online: 5 NOV 2010
- Received 6 May 2010; revised 10 June 2010; accepted 11 June 2010.Final version published online 12 July 2010.
Mitochondria are essential for oxidative energy production in aerobic eukaryotic cells, where they are also required for multiple biosynthetic pathways to take place. Mitochondria also monitor and evaluate complex information from the environment and intracellular milieu, including the presence or absence of growth factors, oxygen, reactive oxygen species, and DNA damage. It follows that disturbances of the integrity of mitochondrial function lead to the disruption of cell function, expressed as disease, aging, or cell death. It has been assumed that the degradation of damaged mitochondria by an autophagy-related pathway specific to mitochondria (mitophagy), recently found to be strictly regulated, is a fundamental process essential for cell homeostasis. Until now, the main role of mitophagy has been tentatively defined as a ‘house-cleaning’ pathway that allows to eliminate altered mitochondria, but mitophagy may also play a role in the adaptation of the number and quality of mitochondria to new environmental conditions. In yeast, recent data defined two categories of mitophagy actors: ones constitutively required for mitophagy and those with mitophagy-regulatory functions. Situations were also uncovered in normal physiology in which cells utilize mitophagy to eliminate damaged, dysfunctional, and superfluous mitochondria to adjust to changing physiological demands.