Fig. 8. An updated model for NC delamination. Opposite the segmental plate mesoderm, high levels of noggin result in low BMP activity, no Wnt1 transcription, low cyclin D1 transcription in dorsal NT and no NC cells emigrating from the caudal NT. N-cadherin at this stage is expressed in the dorsal NT where it contributes to maintaining low cyclin D1 transcription and lack of NC emigration. With ongoing development, opposite mature epithelial and dissociating somites, a factor emitted by the dorsomedial portion of the paraxial mesoderm inhibits noggin transcription in the dorsal NT, thereby releaving BMP activity. 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. In parallel, BMP4, via ADAM10, promotes N-cadherin protein cleavage into CTF1. CTF1 is in turn cleaved by -secretase to generate soluble CTF2. CTF2 may act in at least two ways: by upregulating levels of ß-catenin transcription and by binding ß-catenin protein. We propose that the CTF2-ß-catenin complex translocates into the cell nucleus where transcription of target genes such as cyclin D1, followed by G1-S transition and EMT of NC, are stimulated. Hence, BMP activity transforms N-cadherin from an inhibitory cue into a stimulatory signal. Altogether, these data suggest that NC emigration from the NT is the result of at least two separate yet converging pathways, both stimulated by BMP signaling in coordination with somite development.