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Abstract
The B cell receptor (BCR) and the pre-BCR control cell fate at many stages of B cell development, survival, and antigen response. Most of these processes require the activation of phosphatidylinositol 3-kinase (PI3K). Previous work has pointed to p110δ as the key catalytic isoform of PI3K for many B cell responses. A study of mice with different combinations of PI3K mutations confirms the central role of p110δ in agonist-mediated signaling, while identifying an unexpected function for the p110α isoform in tonic signaling by the pre-BCR and mature BCR.
