Initiates apoptosis in a BH3-independent mechanism possibly by recruiting ced-3 to mitochondria and other cytoplasmic membranes (PubMed:11114722). Has a role in lifespan and tumor growth (PubMed:16380712, PubMed:17934462). Required for the induction of mitophagy under stress conditions (PubMed:25896323). Homodimer; via transmembrane domain (PubMed:11114722, PubMed:9824163). Interacts with ced-3 and ced-9 (PubMed:9824163). Expressed in all somatic tissues including neurons, pharynx, intestine, body wall muscles and vulva muscles. Expressed in the embryo and throughout all stages of development to adulthood. Ubiquitinated and degraded by the proteasome (PubMed:11114722). Under oxidative stress conditions, ubiquitinated at Lys-26 in a pink-1 dependent manner. Colocalizes with pdr-1 and may be ubiquitinated by it (PubMed:25896323). RNAi-mediated knockdown causes an increased sensitivity to stress and inhibits mitophagy which leads to an accumulation of defective mitochondria that have increased mass, altered network morphology, decreased ATP levels, increased reactive oxygen species (ROS) generation, membrane depolarization, increased oxygen consumption and increased cytoplasmic Ca(2+) that intensifies under stress conditions. RNAi-mediated knockdown in daf-2, isp-1, or clk-1 mutant backgrounds suppresses their increased lifespan phenotype. Belongs to the NIP3 family.