Key negative regulator of Shh signaling during neural tube development. Recruited to primary cilia and acts as a regulator of the PKA-dependent basal repression machinery in Shh signaling by increasing cAMP levels, leading to promote the PKA-dependent processing of gli3 into gli3r and repress the Shh signaling. In presence of shh, it is removed from primary cilia, preventing its activity and allowing activation of the Shh signaling (By similarity). Required in left/right patterning by modulating Ca(2+) levels in the cells surrounding the Kupffer vesicle. Mainly localizes to primary cilium and is removed from primary cilia in presence of shh. Expressed throughout embryonic development. At 9- to 16-somites, transcripts are broadly expressed with specific staining observed in the developing nervous system, somites, and precardiac mesoderm. At later stages 1- to 3-days post-fertilization, transcripts become more localized within the dorsal diencephalon, the otic vesicles, and the fin buds. Embryos exhibit perturb cardiac looping as the result of a defect in left/right patterning. Belongs to the G-protein coupled receptor 1 family.