Works in parallel with axl-1 in negatively regulating bar-1 signaling in vulval precursor cells and Q neuroblasts. Inhibits Wnt signaling, which affects tissue specific expression of Hox genes, egl-5, lin-39 and mab-5. This in turn affects QR (postembryonic neuroblast) cell migration, vulval cell fate specification, and the development of sensory structures by the seam cell lineage. Has a role in alae V cell patterning, ray formation in the male tail and axon guidance. Does not affect B cell polarity. Interacts (via N-terminus) with apr-1 (via C-terminus). Interacts with bar-1 (via ARM repeats), gsk-3, and mig-5. Subcellular location was measured using a GFP reporter gene. Location of the pry-1:GFP fusion protein ranges from plasma membrane and cytoplasmic dots to diffuse cytoplasmic and nuclear staining. This difference may be due to variations in expression levels of the fusion protein in different transgenic lines. Expressed in hypodermal cells (seam cells) V5 and V6, Q neuroblasts, ventral hypodermal cells P7/8 to P11/12, body wall muscle cells and neurons in the head, the tail and the ventral nerve cord. Expressed throughout development. Worms exhibit ectopic rays and lack alae in V cells of the male tail. Mutants appear scrawny, often herniated, uncoordinated, show defects in dorsal and ventral cord fasciculation, commissure guidance defects, and over activated Wnt signaling pathway. Phenotypes are more penetrant in the pry-1 and axl-1 double mutant, suggesting some functional overlaps.