Background: Mitochondria are dynamic organelles that frequently change their number, size, shape, and distribution in response to intra- and extracellular cues. After proliferated from pre-existing ones, fresh mitochondria enter constant cycles of fission and fusion that organize them into two distinct states - "individual state" and "network state". When compromised with various injuries, solitary mitochondria are subjected to organelle degradation. This clearance pathway relies on autophagy, a self-eating process that plays key roles in manifold cell activities. Recent studies reveal that defects in autophagic degradation selective for mitochondria (mitophagy) are associated with neurodegenerative diseases, highlighting the physiological relevance to cellular functions.

Scope of review: Here we review recent progress regarding a link between mitochondria and autophagy in yeast and multicellular eukaryotes. In particular, fundamental principles underlying mitophagy, and mitochondrial quality control are emphasized. Accumulating evidence also implicates nonselective autophagy in the management of mitochondrial fitness. Conversely, mitochondria are suggested to serve as signaling platforms vital for regulating autophagy. These interdependent relationships are likely to coordinate metabolic plasticity in the cell.

Major conclusions: Mitochondria and autophagy are elaborately linked homeostatic elements that act in response to changes in cellular environment such as energy, nutrient, and stress. How cells integrate these double membrane-bound systems still remains elusive.

General significance: Interplay between mitochondria and autophagy seems to be evolutionarily conserved. Defects in one of these elements could simultaneously impair the other, resulting in risk increments for various human diseases. This article is part of a Special Issue entitled Biochemistry of Mitochondria.

• PMID: 21846491
• DOI full text
• PubMed

Reference Type

Journal Article | Research Support, Non-U.S. Gov't | Review

Authors

Okamoto K, Kondo-Okamoto N

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