Inactivation of Notch1 impairs VDJbeta rearrangement and allows pre-TCR-independent survival of early alpha beta Lineage Thymocytes.

Détails

ID Serval
serval:BIB_65EE8AB606D8
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Inactivation of Notch1 impairs VDJbeta rearrangement and allows pre-TCR-independent survival of early alpha beta Lineage Thymocytes.
Périodique
Immunity
Auteur(s)
Wolfer A., Wilson A., Nemir M., MacDonald H.R., Radtke F.
ISSN
1074-7613 (Print)
ISSN-L
1074-7613
Statut éditorial
Publié
Date de publication
2002
Volume
16
Numéro
6
Pages
869-879
Langue
anglais
Résumé
Notch proteins influence cell fate decisions in many developmental systems. During lymphoid development, Notch1 signaling is essential to direct a bipotent T/B precursor toward the T cell fate, but the role of Notch1 at later stages of T cell development remains controversial. We have recently reported that tissue-specific inactivation of Notch1 in immature (CD44(-) CD25(+)) thymocytes does not affect subsequent T cell development. Here, we demonstrate that loss of Notch1 signaling at an earlier (CD44(+)CD25(+)) developmental stage results in severe perturbation of alpha beta but not gamma delta lineage development. Immature Notch1(-/-) thymocytes show impaired VDJ beta rearrangement and aberrant pre-TCR-independent survival. Collectively, our data demonstrate that Notch1 controls several nonredundant functions necessary for alpha beta lineage development.
Mots-clé
Animals, Cell Survival, Gene Rearrangement, beta-Chain T-Cell Antigen Receptor/physiology, Integrases/metabolism, Membrane Proteins/physiology, Mice, Mice, Transgenic, Receptor, Notch1, Receptors, Antigen, T-Cell, alpha-beta/physiology, Receptors, Cell Surface, T-Lymphocytes/physiology, Transcription Factors, Viral Proteins/metabolism
Pubmed
Web of science
Open Access
Oui
Création de la notice
28/01/2008 11:39
Dernière modification de la notice
20/08/2019 14:21
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