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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.
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