Ubiquitin-like protein involved in autophagy vesicles formation (By similarity). Conjugation with atg-5 through a ubiquitin-like conjugating system involving also atg-7 as an E1-like activating enzyme and atg-10 as an E2-like conjugating enzyme, is essential for its function (By similarity). Most likely a component of an atg-5-lgg-3-atg-16 complex that promotes autophagosome formation by associating with lgg-2, but not lgg-1, at the preautophagosomal membrane (PubMed:26687600, PubMed:28758895). Probably, as part of an atg-5-lgg-3-atg-16 complex, required for lgg-1 lipidation; the complex acts as an E3-like enzyme promoting atg-3-mediated lgg-1 lipidation (Probable). Involved in the degradation of P-granules by autophagy in somatic cells (PubMed:19167332). This ensures exclusive localization of the P-granules in germ cells (PubMed:19167332). Involved in the elimination of paternal mitochondria in fertilized eggs (PubMed:22105480). Involved in xenophagy, the autophagy-mediated degradation of pathogens and pathogen products, such as toxins (PubMed:27875098). Also plays a role in membrane-pore repair (PubMed:27875098). Most likely a component of a complex at least containing atg-5, lgg-3/ATG12, atg-16.1 and/or atg-16.2 (Probable). Interacts with atg-5 (By similarity). Interacts (via the LIR motif) with lgg-2; the interaction is direct (PubMed:26687600). Recruited to the membrane of autophagic vesicles. Expressed at low levels in embryos. The LIR motif (LC3-interacting region) is required for its interaction with lgg-2. RNAi-mediated knockdown causes no visible phenotype, but animals have a reduced lifespan (PubMed:17204841). Accumulation of pgl-1-positive P granules in somatic cells (PubMed:19167332). Reduced lgg-1-positive autophagosomes in seam cells (PubMed:28758895). Delayed removal of paternal mitochondria in fertilized eggs (PubMed:22105480). RNAi-mediated knockdown reduces autophagic degradation of membrane pore-forming toxin Cry5B. Belongs to the ATG12 family.