Expression data from Gata3+/- and Gata3-/- ESC-derived T-cell progenitors

GATA3 plays a crucial role during early T-cell development and also dictates later T-cell differentiation outcomes. However, its role and collaboration with the Notch signaling pathway in the induction of T-lineage specification and commitment have not been fully elucidated. We show that GATA3 deficiency in hematopoietic progenitors results in an early block in T-cell development despite the presence of Notch signals, with a failure to up-regulate Bcl11b expression, leading to a diversion toward myeloid lineage fate. GATA3 deficiency results in dysregulated Cdkn2b expression, leading to apoptosis of early T-lineage cells due to inhibition of CDK4/6 function. We also show that GATA-3 induces Bcl11b, and together with Bcl11b represses Cdkn2b expression. Our findings provide a signaling and transcriptional network by which the T-lineage program in response to Notch signals is realized. Gata3+/- and Gata3-/- ESCs were maintained in vitro in ES media. ESCs were cultured on OP9/OP9-DL1 cells for differentiation towards the hematopoietic and T-cell lineages. T-cell progenitors were FACS sorted, RNA isolated, and cDNA/cRNA generated for subsequent microarray gene expression analysis.