Wolfer, A.Wilson, A.Nemir, M.MacDonald, H. R.Radtke, F.2006-12-052006-12-052006-12-05200210.1016/S1074-7613(02)00330-8https://infoscience.epfl.ch/handle/20.500.14299/23731212121668Notch 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.AnimalsCell SurvivalGene Rearrangementbeta-Chain T-Cell Antigen Receptor/*physiologyIntegrases/metabolismMembrane Proteins/*physiologyMiceMiceTransgenicReceptorNotch1ReceptorsAntigenT-Cellalpha-beta/*physiology*ReceptorsCell SurfaceResearch SupportNon-U.S. Gov'tT-Lymphocytes/*physiology*Transcription FactorsViral Proteins/metabolismtext::journal::journal article::research article