Have you seen? For parkin, it's not all or nothing

Abstract

Mitochondria accumulate damage over time, which can lead to impairment of cell function by excessive production of reactive oxygen species. The PINK1/Parkin pathway therefore monitors the quality of the mitochondrial population and stimulates the elimination of depolarized organelles by mitophagy. In this issue of The EMBO Journal, McLelland et al (2014) show that this pathway also responds to mild oxidative damage, and instead of inducing mitophagy, allows oxidized proteins to be sorted into mitochondria-derived vesicles (MDVs) that are transported to lysosomes.

Figure 1

Depending on the nature of mitochondrial damage, PINK1 and Parkin will induce mitophagy or the formation of mitochondria-derived vesicles (MDVs) If the damage is severe and depolarizing, mitophagy will be induced. If the damage produces ROS but does not depolarize the mitochondrion, the MDV pathway will be activated instead. PINK1 acts upstream of Parkin in both cases, but with different consequences: either the recruitment of the phagophore to the mitochondrion or the formation MDVs that carry oxidized cargoes to lysosomes. Thus depolarizing insults cause degradation of the entire organelle but ROS triggers degradation of only the selected portions sequestered to the MDVs.