Fig. 9. A model of NC delamination that integrates data from the present and previous studies (see Discussion). Opposite the segmental plate mesoderm, high levels of noggin result in low BMP activity, no Wnt1 transcription, low Cyclin D1 and no NC cells emigrating from the caudal tube. G1/S transition and cell proliferation at this level are independent of BMP/Wnt1. With ongoing development, opposite mature epithelial and dissociating somites, a factor emitted by the dorsomedial region of the paraxial mesoderm inhibits noggin transcription in the dorsal tube, thereby relieving BMP activity from inhibition. BMP4 in turn positively regulates Wnt1 transcription. Wnt signaling, via the canonical pathway, positively modulates transcription of cyclin D1, G1/S transition and NC cell delamination. Maintenance of Pax3, Cad6B and Msx1 transcription in the dorsal tube is also regulated by the BMP/Wnt signaling pathway but their possible involvement in NC delamination awaits further testing. RhoB, at variance, is downstream of BMP but not of Wnt activities. The possible role of RhoB in NC delamination in vivo is still unknown. If it promotes delamination, it might act either via a parallel pathway (pink arrow), be upstream of Wnt1 or of Cyclin D1, or interact at a post-transcriptional level with molecules along the Wnt pathway.