Protease required for deconjugation of smo-1 conjugates from target proteins which is necessary for cell cycle progression (PubMed:25475837) (Probable). Required for respiration and the maintenance of normal mitochondrial homeostasis (PubMed:25187565). In response to mitochondrial stress, required for the removal of smo-1 conjugates from the transcription factor dve-1, which promotes the translocation of dve-1 from the cytosol to the nucleus to initiate the mitochondrial unfolded protein response (PubMed:30642431). Furthermore, removes the smo-1 conjugates from the transcription factor atfs-1 to promote its stability and activate the mitochondrial unfolded protein response (PubMed:30642431). Also plays a role in promoting mitochondrial unfolded protein response-mediated innate immunity following infection with P.aeruginosa (PubMed:30642431). Protein modification; protein sumoylation. Localizes around the metaphase plate and the pericentriolar region and in the surroundings of the central spindle (PubMed:25475837). Translocates from cytoplasm to mitochondrion at late developmental stages (PubMed:25187565). Expressed in hermaphrodite-specific neurons, head muscles, body wall muscles and pharyngeal cells. First expressed in body wall muscles and hypodermal cells during embryonic development to adulthood. Expressed in the pharynx and hypodermis from larval stages L1 to L3. Expressed in hermaphrodite-specific neurons from the L4 stage of larval development. Up-regulated in response to mitochondrial stress induced by antimycin A. Animals are viable, but sterile and display phenotypes including an increased lifespan, age-dependent decline in their pharyngeal pumping rate and locomotion, reduced body fat and decreased oxygen consumption and an impaired ability to maintain mitochondrial membrane potential (PubMed:25187565). RNAi-mediated knockdown causes a number of defects during the first embryonic mitotic division including delayed spindle rotation, diminished spindle pole separation, two-fold faster chromosomal segregation, increased distance between chromosomes after anaphase onset, delayed mitotic exit, less efficient removal of smo-1 from chromatin after anaphase onset and prevention of air-2 from localizing to the spindle midzone (PubMed:25475837). RNAi-mediated knockdown results in increased sumoylation of hmgs-1 (PubMed:25187565). RNAi-mediated knockdown prevents dve-1 translocation to the nucleus in response to mitochondrial stress (PubMed:30642431). RNAi-mediated knockdown reduces the levels of afts-1, but levels are restored following inhibition of the proteasome (PubMed:30642431). RNAi-mediated knockdown reduces the survival of animals and results in impaired activation of the mitochondrial unfolded protein response following the inhibition of respiration induced by antimycin A (PubMed:30642431). RNAi-mediated knockdown impairs development and survival, and reduces the expression of immune response genes lys-2, zip-2, clec-4, clec-65 and ugt-61 following infection with P.aeruginosa (PubMed:30642431). Belongs to the peptidase C48 family.