Deubiquitinating enzyme that acts as an inhibitor of mitophagy probably by counteracting the action of park. Possibly functions by hydrolyzing ubiquitin attached by park on target proteins, thereby reducing park's ability to drive mitophagy. Thiol-dependent hydrolysis of ester, thioester, amide, peptide and isopeptide bonds formed by the C-terminal Gly of ubiquitin (a 76-residue protein attached to proteins as an intracellular targeting signal). RNAi-mediated knockdown has no effect on the number of mitochondrial clumps and mitochondrial membrane potential in the indirect flight muscles, and there is also no effect on climbing performance. However RNAi-mediated knockdown rescues the defective mitophagy phenotypes caused by mutations in park; reducing the number of mitochondrial clumps, and improving mitochondrial membrane potential and climbing performance in park-deficient flies. Belongs to the peptidase C19 family. USP20/USP33 subfamily.