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Protein degradation

An alternative route for mitochondrial quality control

Nature Reviews Molecular Cell Biology volume 15, pages 150–151 (2014)Cite this article

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The authors previously reported that oxidative stress induces the biogenesis of a subpopulation of mitochondria-derived vesicles (MDVs) that selectively targets oxidized cargo for lysosomal degradation; now, they investigated the involvement of parkin in this pathway.

They analysed the subcellular localization of GFP-tagged parkin in mammalian cells that were defective in mitochondrial fission and that are thus unable to affect mitophagy. When treating the cells with antimycin A, which causes the formation of mitochondrial reactive oxygen species (ROS), GFP–parkin was rapidly recruited to nascent, budding vesicles at the periphery of mitochondria. Such vesicles were not observed in unstimulated cells, which suggests that parkin promotes MDV biogenesis in response to mitochondrial ROS. Moreover, ROS-induced formation of MDVs was inhibited in PINK1-depleted cells, indicating that both parkin and PINK1 are required in this process.

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References

  1. McLelland, G.-L. et al. Parkin and PINK1 function in a vesicular trafficking pathway regulating mitochondrial quality control. EMBO J. http://dx.doi.org/10.1002/embj.201385902 (2014)

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  1. Andrea Du Toit
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Du Toit, A. An alternative route for mitochondrial quality control. Nat Rev Mol Cell Biol 15, 150–151 (2014). https://doi.org/10.1038/nrm3755

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