Metalloprotease involved in molting, a process during larval stages in which a new cuticle is formed and the old cuticle is shed (PubMed:24957743). Plays a role in thermotolerance probably by preventing the accumulation of oxidized lipoproteins and cholesterol (PubMed:20600277, PubMed:24957743). Inhibited by human TIMP1 and TIMP2 and the broad MMP inhibitors BB94 (Batimastat) and CT543. Expressed in spermatheca and spermathecal-uterine valve, weakly in vulva and anal muscles and in two cells in the head (probably RMEV and RMED motor neurons). Expressed at the comma, 1.5-fold and 3-fold embryonic stages in multiple cells including muscle and somatic gonad cells. In L1 larvae, predominantly expressed in specific muscles and somatic gonad cells, in L2 larvae predominantly expressed in muscles cells and in L4 larvae expressed predominantly in the developing spermatheca and more weakly in vulva muscle cells. Expression increases in the hypodermis in dauer stage larvae prior molting to L4 larval stage. The conserved cysteine present in the cysteine-switch motif binds the catalytic zinc ion, thus inhibiting the enzyme. The dissociation of the cysteine from the zinc ion upon the activation-peptide release activates the enzyme. RNAi-mediated knockdown causes a delay in larval to adult development with reduced motility and feeding (PubMed:20600277). Also reduces fecundity in adults (PubMed:20600277). Larvae have molting defects characterized by incomplete cuticle shedding leaving a constriction ring in the larvae anterior part (PubMed:20600277). Reduces survival upon Gram-negative bacterium P.luminescense infection or heat stress (PubMed:20600277, PubMed:24957743). Production of extra- and intra-cellular reactive oxygen species (ROS) and protein oxidation are increased whereas vit-6 transcription and dehydroergosterol (DHE) uptake are reduced (PubMed:24957743). Moreover, causes constitutive daf-16 nuclear localization (PubMed:24957743). Simultaneous RNAi-mediated knockdown of vit-6, rme-2, daf-16 or daf-16 coactivators sir2.1, ftt-2 and par-2 restores normal thermotolerance (PubMed:24957743). RNAi-mediated knockdown in a daf-9 or daf-12 mutant background reduces survival further upon heat stress. Belongs to the peptidase M10A family. Intron retention.