The pathways of mitophagy for quality control and clearance of mitochondria

@article{Ashrafi2013ThePO,
  title={The pathways of mitophagy for quality control and clearance of mitochondria},
  author={Ghazaleh Ashrafi and Thomas L. Schwarz},
  journal={Cell Death and Differentiation},
  year={2013},
  volume={20},
  pages={31-42}
}
Selective autophagy of mitochondria, known as mitophagy, is an important mitochondrial quality control mechanism that eliminates damaged mitochondria. Mitophagy also mediates removal of mitochondria from developing erythrocytes, and contributes to maternal inheritance of mitochondrial DNA through the elimination of sperm-derived mitochondria. Recent studies have identified specific regulators of mitophagy that ensure selective sequestration of mitochondria as cargo. In yeast, the mitochondrial… 

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References

SHOWING 1-10 OF 112 REFERENCES

Mitophagy in cells with mtDNA mutations

The Parkinson disease-related proteins PINK1 and PARK2 (PARKIN, a cytosolically-localized E3 ubiquitin ligase) are essential for targeting mitochondria for mitophagy, and upon chemical uncoupling of the mitochondrial transmembrane potential, Pink1 located in the mitochondrial outer membrane recruits PARK2 from the cytosoli to the mitochondria, followed by delivery of the organelle to the autophagic machinery for degradation.

Atg32 is a mitochondrial protein that confers selectivity during mitophagy.

Mitochondria autophagy in yeast.

Recent advances in the physiology and molecular mechanism of mitophagy are reviewed and the similarities and differences of this degradation process between yeast and mammalian cells are discussed.

Mitophagy in Yeast Occurs through a Selective Mechanism*

A new method is developed to detect mitochondrial autophagy (mitophagy) by fusing the green fluorescent protein at the C terminus of two endogenous mitochondrial proteins and monitored vacuolar release of green fluorescentprotein, which suggests that the degradation of mitochondria is a tightly regulated process and that these organelles are largely protected from nonspecific autophagic degradation.

Nix Is Critical to Two Distinct Phases of Mitophagy, Reactive Oxygen Species-mediated Autophagy Induction and Parkin-Ubiquitin-p62-mediated Mitochondrial Priming*

This work distinguished the molecular events responsible for the different phases of mitophagy and placed Nix upstream of the events, finding that Nix was required for the autophagy induction.

Drosophila Parkin requires PINK1 for mitochondrial translocation and ubiquitinates Mitofusin

It is shown in Drosophila cells that PINK1 is required to recruit Parkin to dysfunctional mitochondria and promote their degradation, and Mfn ubiquitination may provide a mechanism by which terminally damaged mitochondria are labeled and sequestered for degradation by autophagy.

Broad activation of the ubiquitin–proteasome system by Parkin is critical for mitophagy

It is shown that upon translocation to mitochondria, Parkin activates the ubiquitin–proteasome system (UPS) for widespread degradation of outer membrane proteins, and remodeling of the mitochondrial outer membrane proteome is important for mitophagy, and a causal link between the UPS and autophagy is revealed.

Impairing the bioenergetic status and the biogenesis of mitochondria triggers mitophagy in yeast

It is shown that, in yeast cells grown under nonstarving conditions, autophagy can be induced by mitochondrial dysfunction, and mitochondrial damage-induced Autophagy results in the preferential degradation of impaired mitochondria (mitophagy), before leading to cell death.

Structures containing Atg9A and the ULK1 complex independently target depolarized mitochondria at initial stages of Parkin-mediated mitophagy

Analysis of the recruitment of Atg proteins in Parkin-dependent mitophagy suggests a process whereby the isolation membrane is generated de novo on damaged mitochondria as opposed to one where a preformed isolation membrane recognizes mitochondria.
...