Ligand for members of the frizzled family of seven transmembrane receptors (By similarity). Shares much functionality with wnt11b. Signals through a non-canonical Wnt pathway to activate Jun-N-terminal kinase (JNK) to regulate gastrulation movements. Acts in a non-cell-autonomous manner to control neural crest migration, probably acting as an extracellular signal from surrounding tissue, but is not required for neural crest induction. Acts redundantly with wnt11b during pronephros induction. Regulates cardiac morphogenesis through the activation of JNK, but is not required for cardiac differentiation. Essential for dorsal fin development; required for an epithelial to mesenchymal transformation event prior to migration of cells into the fin, and ultimately for maintenance of fin structure. Mediates dorsal fin development through a non-canonical pathway mediated by Ca(2+). In embryos, expressed in the neural tube, dorsal somite, mesenchymal cells within the dorsal fin, branchial arches and heart muscle, becoming expressed throughout the myocardium by the tadpole stage (stage 45). Prior to neural crest cell migration, expressed in a domain flanking the neural crest on the medial or neural (the opposite side to wnt11b). Weakly expressed in the developing pronephros from stage 25, with expression increasing from stages 30 to 35. Expressed after gastrulation (post stage 13). Glycosylation is required for protein secretion. Palmitoleoylation is required for efficient binding to frizzled receptors. Depalmitoleoylation leads to Wnt signaling pathway inhibition. Xenopus and other lower vertebrates contain duplicated wnt11 genes resulting from an ancient gene duplication event, but the second copy has since been lost in mammals. This gene was originally called wnt11r (PubMed:8306880). but was renamed to wnt11 to reflect its orthology (PubMed:17436276). Belongs to the Wnt family.