Skip Navigation



Human Molecular Genetics Advance Access published online on August 8, 2008
Human Molecular Genetics, doi:10.1093/hmg/ddn235
This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow Supplementary Data
Right arrowOA All Versions of this Article:
17/21/3411    most recent
ddn235v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Google Scholar
Right arrow Articles by Thomas, S.
Right arrow Articles by Etchevers, H. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Thomas, S.
Right arrow Articles by Etchevers, H. C.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 2008 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Human neural crest cells display molecular and phenotypic hallmarks of stem cells

Sophie Thomas1, Marie Thomas1, Patrick Wincker2, Candice Babarit1, Puting Xu3, Marcy C. Speer3,{dagger}, Arnold Munnich1,4, Stanislas Lyonnet1,4, Michel Vekemans1,4 and Heather C. Etchevers1,5,*

1 INSERM, U781, Hôpital Necker - Enfants Malades, 149 rue de Sèvres, 75015 Paris, France 2 GENOSCOPE (CEA) and UMR 8030 CNRS-GENOSCOPE-Université d'Evry, 2 rue Gaston Crémieux, 91057 Evry, France 3 Center for Human Genetics, Department of Medicine, Duke University Medical Center, Durham, North Carolina, 27710, USA 4 Université Paris Descartes, Faculté de Médecine, 15 rue de l'Ecole de Médecine, 75005 Paris, France 5 INSERM, U563, Centre de Physiopathologie de Toulouse - Purpan, 31300 Toulouse, France

* Corresponding author. Fax: +33 5 62 74 45 58. Telephone: +33 5 62 74 45 87. heather.etchevers{at}inserm.fr

Received June 23, 2008; Revised August 6, 2008; Accepted August 6, 2008

The fields of developmental and stem cell biology both explore how functionally distinct cell types arise from a self-renewing founder population. Multipotent, proliferative human neural crest cells (hNCC) develop toward the end of the first month of pregnancy. It is assumed that most differentiate after migrating throughout the organism, although in animal models neural crest stem cells reportedly persist in postnatal tissues. Molecular pathways leading over time from an invasive mesenchyme to differentiated progeny such as the dorsal root ganglion, the maxillary bone or the adrenal medulla are altered in many congenital diseases. To identify additional components of such pathways, we derived and maintained self-renewing hNCC lines from pharyngulas. We show that, unlike their animal counterparts, hNCC are able to self-renew ex vivo under feeder-free conditions. While cross species comparisons showed extensive overlap between human, mouse and avian NCC transcriptomes, some molecular cascades are only active in the human cells, correlating with phenotypic differences. Furthermore, we found that the global hNCC molecular profile is highly similar to that of pluripotent embryonic stem cells as compared with other stem cell populations or hNCC derivatives. The pluripotency markers NANOG, POU5F1 and SOX2 are also expressed by hNCC, and a small subset of transcripts can unambiguously identify hNCC among other cell types. The hNCC molecular profile is thus both unique and globally characteristic of uncommitted stem cells.

{dagger} Died August 4, 2007


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Proc. Natl. Acad. Sci. USAHome page
L. de Pontual, N. A. Zaghloul, S. Thomas, E. E. Davis, D. M. Mcgaughey, H. Dollfus, C. Baumann, S. L. Bessling, C. Babarit, A. Pelet, et al.
Epistasis between RET and BBS mutations modulates enteric innervation and causes syndromic Hirschsprung disease
PNAS, August 18, 2009; 106(33): 13921 - 13926.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.