Mice deficient for the pre-TCRα (pTα) chain cannot form a pre-T cell receptor (TCR) and exhibit a severe defect in early T cell development, characterized by lack of "β selection" and impaired generation of double-positive (DP) thymocytes. Here, we demonstrate that intraperitoneal injection of CD3ε-specific antibodies into pTα^−/− × RAG^−/− mice or introduction of an activated p56 ^lck transgene in pTα^−/− mice fully restores the number of DP thymocytes, and that expression of a transgenic pTα chain lacking its cytoplasmic portion can overcome all developmental defects associated with pTα deficiency. These results allow a better definition of the role of pTα in pre-TCR signal transduction and provide conclusive evidence that the cytoplasmic tail of pTα is not essential for pre-TCR signaling.