| First Author | Wolfer A | Year | 2002 |
| Journal | Immunity | Volume | 16 |
| Issue | 6 | Pages | 869-79 |
| PubMed ID | 12121668 | Mgi Jnum | J:77524 |
| Mgi Id | MGI:2181924 | Doi | 10.1016/s1074-7613(02)00330-8 |
| Citation | Wolfer A, et al. (2002) Inactivation of Notch1 Impairs VDJbeta Rearrangement and Allows pre-TCR-Independent Survival of Early alphabeta Lineage Thymocytes. Immunity 16(6):869-79 |
| abstractText | 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 alphabeta but not gammadelta lineage development. Immature Notch1(-/-) thymocytes show impaired VDJbeta rearrangement and aberrant pre-TCR-independent survival. Collectively, our data demonstrate that Notch1 controls several nonredundant functions necessary for alphabeta lineage development. |
