The Igg1 B-Cell Receptor Provides Survival And Proliferative Signals Analogue To The Ig Alpha But Not The Ig Beta Co-Receptor

The function of the IgM B-cell receptor (BCR) is dependent on intact signaling of the co-receptors Ig alpha and Ig beta, both ofwhich contain a cytoplasmic tail bearing an immunoreceptor tyrosine-based activation motif. We have previously demonstrated that the cytoplasmic tail of the IgG1 BCR can partially compensate for the loss of the signaling moiety of Ig alpha. Here, we show that unlike Ig alpha, Ig beta signaling is indispensable for the development and function of IgG1-expressing B cells. Deletion of the cytoplasmic signaling tail of Ig beta compromised the survival and proliferation not only of IgM(+) B cells but also of IgG1-expressing B cells. In the absence of the signaling tail of Ig beta, the transcription levels of the antiapoptotic gene bcl-xl and the cell-cycle gene ccnd2 were reduced, consistent with the observed defects in survival and proliferation. These results demonstrate functional differences between Ig alpha and Ig beta in the transduction of IgG1 BCR signal.