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First published online 15 April 2009
doi: 10.1242/dev.028373

Development 136, 1717-1726 (2009)
Published by The Company of Biologists 2009
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Role of noggin as an upstream signal in the lack of neuronal derivatives found in the avian caudal-most neural crest

Liliana Osório1,2,3,*,{dagger}, Marie-Aimée Teillet1,2 and Martin Catala1,2

1 UPMC Univ Paris 06, UMR 7622, Laboratoire de Biologie du Développement, F-75005, Paris, France.
2 CNRS, UMR 7622, Laboratoire de Biologie du Développement, F-75005, Paris, France.
3 Life and Health Sciences Research Institute, School of Health Sciences, University of Minho, 4710-057 Braga, Portugal.

{dagger} Author for correspondence (e-mail: liliana.osorio-da-silva{at}snv.jussieu.fr)

Accepted 13 March 2009

Neural crest cells (NCCs) arising from trunk neural tube (NT) during primary and secondary neurulation give rise to melanocytes, glia and neurons, except for those in the caudal-most region during secondary neurulation (somites 47 to 53 in the chick embryo), from which no neurons are formed, either in vivo or in vitro. To elucidate this discrepancy, we have specifically analyzed caudal-most NCC ontogeny. In this region, NCCs emerge at E5/HH26, one day after full cavitation of the NT and differentiation of flanking somites. The absence of neurons does not seem to result from a defect in NCC specification as all the usual markers, with the exception of Msx1, are expressed in the dorsal caudal-most NT as early as E4/HH24. However, Bmp4-Wnt1 signaling, which triggers trunk NCC delamination, is impaired in this region due to persistence of noggin (Nog) expression. Concomitantly, a spectacular pattern of apoptosis occurs in the NT dorsal moiety. Rostral transplantation of either the caudal-most somites or caudal-most NT reveals that the observed features of caudal-most NCCs relate to properties intrinsic to these cells. Furthermore, by forced Nog expression in the trunk NT, we can reproduce most of these particular features. Conversely, increased Bmp4-Wnt1 signaling through Nog inhibition in the caudal-most NT at E4/HH24 induces proneurogenic markers in migratory NCCs, suggesting that noggin plays a role in the lack of neurogenic potential characterizing the caudal-most NCCs.

Key words: Apoptosis, Chick, Delamination, Msx1, Noggin, Wnt1, Neural crest, Neuronal differentiation


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© The Company of Biologists Ltd 2009