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Cited by 212

The DOI matches its Crossref record.

Antagonistic roles of full-length N-cadherin and its soluble BMP cleavage product in neural crest delamination

Shoval, Irit, Ludwig, Andreas, Kalcheim, Chaya·2007·Development
DOI 10.1242/dev.02742
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Abstract

During neural crest ontogeny, an epithelial to mesenchymal transition is necessary for cell emigration from the dorsal neural tube. This process is likely to involve a network of gene activities, which remain largely unexplored. We demonstrate that N-cadherin inhibits the onset of crest delamination both by a cell adhesion-dependent mechanism and by repressing canonical Wnt signaling previously found to be necessary for crest delamination by acting downstream of BMP4. Furthermore, N-cadherin protein,but not mRNA, is normally downregulated along the dorsal tube in association with the onset of crest delamination, and we find that this process is triggered by BMP4. BMP4 stimulates cleavage of N-cadherin into a soluble cytoplasmic fragment via an ADAM10-dependent mechanism. Intriguingly, when overexpressed, the cytoplasmic N-cadherin fragment translocates into the nucleus, stimulates cyclin D1 transcription and crest delamination, while enhancing transcription of β-catenin. CTF2 also rescues the mesenchymal phenotype of crest cells in ADAM10-inhibited neural primordia. Hence, by promoting its cleavage, BMP4 converts N-cadherin inhibition into an activity that is likely to participate, along with canonical Wnt signaling, in the stimulation of neural crest emigration.

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Metadata

Authors
Shoval, I., Ludwig, A., & Kalcheim, C.
Venue
Development
Publisher
The Company of Biologists
Published
2007-02-01
Volume
134
Issue
3
Pages
491-501
ISSN
  • 0950-1991 (ISSN-L)
  • 1477-9129
DOI
10.1242/dev.02742
OpenAlex
W2111761019
Cited by
212
References
0
FWCI
4.91
Type
journal article
Language
en
Open access
closed

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