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First published online 29 September 2004
doi: 10.1242/dev.01424

Development 131, 5327-5339 (2004)
Published by The Company of Biologists 2004
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Canonical Wnt activity regulates trunk neural crest delamination linking BMP/noggin signaling with G1/S transition

Tal Burstyn-Cohen, Jonathan Stanleigh, Dalit Sela-Donenfeld* and Chaya Kalcheim{dagger}

Department of Anatomy and Cell Biology, Hebrew University-Hadassah Medical School, PO Box 12272, Jerusalem 91120, Israel

{dagger} Author for correspondence (e-mail: kalcheim{at}nn-shum.cc.huji.ac.il)

Accepted 31 August 2004

Delamination of premigratory neural crest cells depends on a balance between BMP/noggin and on successful G1/S transition. Here, we report that BMP regulates G1/S transition and consequent crest delamination through canonical Wnt signaling. Noggin overexpression inhibits G1/S transition and blocking G1/S abrogates BMP-induced delamination; moreover, transcription of Wnt1 is stimulated by BMP and by the developing somites, which concomitantly inhibit noggin production. Interfering with ß-catenin and LEF/TCF inhibits G1/S transition, neural crest delamination and transcription of various BMP-dependent genes, which include Cad6B, Pax3 and Msx1, but not that of Slug, Sox9 or FoxD3. Hence, we propose that developing somites inhibit noggin transcription in the dorsal tube, resulting in activation of BMP and consequent Wnt1 production. Canonical Wnt signaling in turn stimulates G1/S transition and generation of neural crest cell motility independently of its proposed role in earlier neural crest specification.

Key words: Avian embryo, Cell cycle, Cyclin D1, Epithelial to mesenchymal transition, Neural tube, Somite


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