Ubiquitin-like modifier involved in the formation of autophagosomal vacuoles (autophagosomes) (PubMed:26687600). When lipidated mediates tethering between adjacent membranes and stimulates membrane fusion during autophagy (PubMed:26687600, PubMed:21802374). Recruits lipidated-lgg-2 to maturing autophagosomes (PubMed:12958363, PubMed:20523114, PubMed:26687600). Acts in the aggrephagy pathway, which is the macroautophagic degradation of ubiquitinated protein aggregates, and preferentially interacts with autophagy proteins and substrates containing LIR motifs to mediate autophagosome formation and protein aggregate degradation (PubMed:26687600). In particular, binds to components of the unc-51-atg-13 complex to regulate autophagosome formation and cargo sequestration (PubMed:26687600). Required for the degradation of specific sepa-1- and sqst-1-containing protein aggregates during embryogenesis (PubMed:26687600). Involved in allophagy, which is an autophagic process in which paternal mitochondria and organelles are degraded during fertilization, and moreover is required for the formation of lgg-2-positive allophagic autophagosomes in embryos (PubMed:24374177). Involved in the clearance of apoptotic cells by promoting the delivery of engulfed apoptotic cells to the lysosome (PubMed:22451698). Plays a role in the distribution and clearance of germ cell specific P-granules from somatic cells (PubMed:19167332). Also plays a role in the autophagy-mediated degradation of ribosomal RNA and ribosomal proteins in lysosomes (PubMed:30102152). Involved in xenophagy, the autophagy-mediated degradation of pathogens and pathogen products, such as toxins (PubMed:27875098). Required for normal survival when exposed to pathogenic bacteria S.typhimurium probably by promoting autophagic degradation of intracellular S.typhimurium (PubMed:19667176). Also plays a role in membrane-pore repair (PubMed:27875098). Plays a role in mitophagy (PubMed:25896323). Essential for dauer development and longevity, including longevity in response to moderate, short-term heat shock, also known as a hormetic heat shock (PubMed:12958363, PubMed:20523114, PubMed:28198373). Interacts with sepa-1 (via the LIR motifs); the interaction is direct (PubMed:19167332, PubMed:26687600). Interacts with allo-1 (via the LIR motif) (PubMed:29255173). Interacts with sqst-1 (via the LIR motifs); the interaction is direct (PubMed:26687600). Both lipidated and unlipidated forms interact with epg-7 (via the LIR motif); the interaction is direct (PubMed:26687600). Interacts with epg-2 (via the LIR motifs); the interaction is direct (PubMed:26687600). Interacts with atg-13; the interaction is direct (PubMed:26687600). Interacts with unc-51 (via the LIR motif); the interaction is direct (PubMed:26687600). Interacts with atg-7; the interaction is direct (PubMed:26687600). Interacts with atg-3 (PubMed:26687600). The interaction with atg-7 and atg-3 may be required for the lipidation of lgg-1 (PubMed:26687600). In embryos, diffuse cytoplasmic localization with some areas displaying a more punctate distribution (PubMed:19377305, PubMed:19167332, PubMed:24374177, PubMed:28806108, PubMed:20550938). Specifically, upon fertilization localizes to autophagosomes around the male pronucleus (PubMed:24374177). During the first embryonic divisions and after the 25-cell stage, localizes to a large population of autophagosomes, with another smaller population of autophagosomes containing both lgg-1 and lgg-2 (PubMed:24374177). Localization to autophagosomes is dependent on atg-7 (PubMed:24374177). Co-localizes with sepa-1 in cytoplasmic aggregates (PubMed:19167332, PubMed:28806108). Partially localizes to the phagosome membrane of engulfed apoptotic cells (PubMed:22451698). Expressed in PLML touch receptor neuron and in the ventral nerve cord (PubMed:17327275). Expressed in AIY interneurons (PubMed:30880001). Expressed during embryogenesis (PubMed:19167332, PubMed:24374177, PubMed:28806108, PubMed:20550938, PubMed:24185444, PubMed:26687600). First expressed at the 20 cell stage with expression peaking at the 80-100 cell stage, and decreasing as development continues (PubMed:20550938, PubMed:24185444, PubMed:28806108, PubMed:22767594). Undetectable at the comma stage (PubMed:28806108). Induced in response to a moderate, short-term heat stess, also known as a hormetic heat stess. Cleaved by atg-4.1 and/or atg-4.2, after Gly-116 to form a thioester bond with 'Cys-523' of atg-7 (E1-like activating enzyme) before being transferred to 'Cys-255' of atg-3 (E2 conjugating enzyme), in order to be amidated with phosphatidylethanolamine (Probable) (PubMed:26687600, PubMed:22767594). This lipid modification anchors lgg-1 to membranes and can be reversed by atg-4.2, releasing soluble lgg-1 (PubMed:30880001). Lipidation regulates lgg-2-positive autophagosome formation (PubMed:26687600). RNAi-mediated knockdown prevents mitophagy (PubMed:25896323). Accumulation of germ cell specific P-granules in somatic cells as indicated by increased numbers of pgl-1 and pgl-3 positive granules in embryos and L1 stage larva (PubMed:19167332). RNAi-mediated knockdown results in increased numbers of sepa-1- and lgg-2-expressing protein aggregates in embryos (PubMed:26687600). RNAi-mediated knockdown reduces autophagic degradation of membrane pore-forming toxin Cry5B (PubMed:27875098). Impaired survival when exposed to pathogenic bacteria S.typhimurium (PubMed:19667176). Reduces the number of vacuolated (dying) touch receptor neurons in a mec-4 u231, deg-1 u506 or deg-3 u662 mutants (PubMed:17327275). The extended lifespan of animals exposed to hormetic heat shock early in life is significantly reduced by RNAi-mediated knockdown. Belongs to the ATG8 family.