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Goosecoid (Gsc ) expression marks the primary embryonic organizer in vertebrates and beyond. While functions have been assigned during later embryogenesis, the role of  Gsc  in the organizer has remained enigmatic. Using conditional gain-of-function approaches in  Xenopus  and mouse to maintain  Gsc  expression in the organizer and along the axial midline, neural tube closure defects (NTDs) arose and dorsal extension was compromised. Both phenotypes represent convergent extension (CE) defects, arising from impaired Wnt/planar cell polarity (PCP) signaling. Dvl2 recruitment to the cell membrane was inhibited by Gsc in  Xenopus  animal cap assays and key Wnt/PCP factors ( RhoA, Vangl2, Prickle, Wnt11 ) rescued Gsc-mediated NTDs. Re-evaluation of endogenous  Gsc  functions in MO-mediated gene knockdown frog and knockout mouse embryos unearthed PCP/CE-related phenotypes as well, including cartilage defects in  Xenopus  and misalignment of inner ear hair cells in mouse. Our results assign a novel function to  Gsc  as an inhibitor of Wnt/PCP-mediated CE. We propose that in the organizer  Gsc  represses CE as well:  Gsc -expressing prechordal cells, which leave the organizer first, migrate and do not undergo CE like the  Gsc -negative notochordal cells, which subsequently emerge from the organizer. In this model,  Gsc  provides a switch between cell migration and CE, i.e. cell intercalation.

A novel role of the organizer gene Goosecoid as an inhibitor of Wnt/PCP-mediated convergent extension in Xenopus and mouse