Probable ligand for lin-12/Notch and glp-1/Notch receptors and involved in the mediation of Notch signaling (PubMed:8139658, PubMed:7607081, PubMed:18036582, PubMed:18700817, PubMed:8575327). Involved in the lin-12/Notch pathway signaling of cell fate in vulval precursor cells (VPCs) and in the postembryonic mesodermal lineage (M lineage), acting redundantly with dsl-1 and apx-1 (PubMed:14960273, PubMed:18036582). Functions in uterine cells to promote basement membrane mobility during tissue remodeling (PubMed:27661254, PubMed:8139658). Required for oocyte growth control, acting redundantly with apx-1, perhaps signaling via the glp-1/Notch pathway (PubMed:19502484). Plays a role in Notch-dependent induction of left-right asymmetry in interneurons and motoneurons (PubMed:21737278). Involved in maintaining the developmentally arrested larval state known as dauer, probably signaling in the glp-1/Notch pathway (PubMed:18599512). Required for normal sleep bout quantity and arousal thresholds during the transition from the last larval stage to adulthood in well-fed animals (PubMed:29523076). May interact with lin-12 / Notch receptor. Expressed in the gonad distal tip cell (DTC) of hermaphrodites. Expressed in cells immediately adjacent to ventral mesodermal lineage (M lineage) cells, but not next to dorsal M lineage cells, beginning at the 4-M stage (PubMed:18036582). Expressed in all six vulval precursor cells (VPCs) in the early larval L3 stage, subsequently more highly expressed in P6.p while the expression in the other VPCs diminishes (PubMed:14960273, PubMed:21596897). Expressed in the anchor cell (AC) and distal tip cells (DTCs) of the somatic gonad at larval stage L3 (PubMed:21596897). Expressed in the inter labial IL2 neurons at the onset of and throughout the developmentally arrested larval state known as dauer (PubMed:18599512). The N-terminal region and DSL domain may be involved in interacting with Notch receptors. RNAi-mediated knockdown in cells of the pi uterine cell lineage results in impaired basement membrane mobility (PubMed:27661254). RNAi-mediated knockdown, on a lin-15 mutant background, causes adjacent vulval precursor cells (VPCs) to adopt altered cell fate (PubMed:14960273). RNAi-mediated knockdown, when combined with knockdown of apx-1, on a dsl-1 mutant background, causes adjacent vulval precursor cells (VPCs) to adopt altered cell fate; phenotype exacerbated on double mutant lin-15;dsl-1 background (PubMed:14960273). RNAi-mediated knockdown, on a lin-12 mutant background, induces the presence of 1-2 extra mesodermal lineage (M lineage)-derived coelomocytes and the concomitant loss of sex myoblasts on the ventral side of the animal (PubMed:18036582). On an apx-1 mutant background, RNAi-mediated knockdown causes germ cells to display nuclear morphology consistent with meiotic prophase or gametogenesis in adult hermaphrodites (PubMed:19502484).