Rhes, a striatal-enriched protein, promotes mitophagy via Nix

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Significance Damaged mitochondria are eliminated by lysosomes, a process called mitophagy. However, the brain tissue specific roles and mechanisms of mitophagy remain unknown. We report that Rhes, a protein highly enriched in the striatum, eliminates damaged mitochondria via mitophagy, a function that may regulate the optimum number and function of mitochondria in the striatum. However, when mitochondria are irreversibly damaged, as in the presence of 3-NP (an inhibitor of complex II, SDH), Rhes exacerbates mitophagy in association with Nix, a mitophagy receptor and promotes cell death. Intriguingly, Rhes can travel via membranous protrusions from a healthy cell to the neighboring cell and interacts with the damaged mitochondria via Nix. Collectively, Rhes acts as “mitochondrial surveillant,” and excessive mitophagy may account for striatal vulnerability in brain.