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Whereas Tcf1\n            <jats:sup>\u2212<\/jats:sup>\n            ETPs exhibited higher proliferative capacity, Tcf1\n            <jats:sup>+<\/jats:sup>\n            ETPs appeared to be immediate, more robust precursors to T lineage\u2013specified early thymocytes. Prethymic ablation of Tcf1 and its homolog Lef1 severely impaired ETP formation in vivo. Whereas ablating Tcf1 alone had limited impact, loss of both Tcf1 and Lef1 impaired transcriptional activation of\n            <jats:italic toggle=\"yes\">Notch1<\/jats:italic>\n            and Notch pathway effector molecules, including\n            <jats:italic toggle=\"yes\">Hes1<\/jats:italic>\n            and\n            <jats:italic toggle=\"yes\">Hhex<\/jats:italic>\n            , accompanied by aberrantly induced B cell and myeloid gene programs. Acute deletion of both factors compromised Notch pathway, glycolysis, and T cell gene programs in emergent ETPs ex vivo. 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