Control of hair follicle cell fate by underlying mesenchyme through a CSL-Wnt5a-FoxN1 regulatory axis.

Détails

ID Serval
serval:BIB_42D8EECD68E5
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Control of hair follicle cell fate by underlying mesenchyme through a CSL-Wnt5a-FoxN1 regulatory axis.
Périodique
Genes and Development
Auteur(s)
Hu B., Lefort K., Qiu W., Nguyen B.C., Rajaram R.D., Castillo E., He F., Chen Y., Angel P., Brisken C., Dotto G.P.
ISSN
1549-5477[electronic], 0890-9369[linking]
Statut éditorial
Publié
Date de publication
2010
Peer-reviewed
Oui
Volume
24
Numéro
14
Pages
1519-1532
Langue
anglais
Résumé
Epithelial-mesenchymal interactions are key to skin morphogenesis and homeostasis. We report that maintenance of the hair follicle keratinocyte cell fate is defective in mice with mesenchymal deletion of the CSL/RBP-Jkappa gene, the effector of "canonical" Notch signaling. Hair follicle reconstitution assays demonstrate that this can be attributed to an intrinsic defect of dermal papilla cells. Similar consequences on hair follicle differentiation result from deletion of Wnt5a, a specific dermal papilla signature gene that we found to be under direct Notch/CSL control in these cells. Functional rescue experiments establish Wnt5a as an essential downstream mediator of Notch-CSL signaling, impinging on expression in the keratinocyte compartment of FoxN1, a gene with a key hair follicle regulatory function. Thus, Notch/CSL signaling plays a unique function in control of hair follicle differentiation by the underlying mesenchyme, with Wnt5a signaling and FoxN1 as mediators.
Mots-clé
Animals, Forkhead Transcription Factors/metabolism, Gene Deletion, Hair Follicle, Immunoglobulin J Recombination Signal Sequence-Binding Protein/metabolism, Keratinocytes/metabolism, Mice, Signal Transduction, Wnt Proteins/genetics, Wnt Proteins/metabolism
Pubmed
Web of science
Création de la notice
14/09/2010 15:29
Dernière modification de la notice
03/03/2018 16:39
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