The pre-B cell receptor (pre-BCR) and the BCR are required for B lymphopoiesis and for the allelic exclusion of Ig genes. Mice lacking B cell linker (BLNK) protein that is a component of the BCR signaling pathway have impaired Il cell development, In this report, we show that allelic exclusion is intact in BLNK-/- mice harboring a V(H)12 transgene, This differs from mice lacking the tyrosine kinase Syk that is upstream of BLNK in BCR signaling and contrasts with mice lacking SLP-76 that is the equivalent adaptor molecule in TCR-signal transduction, We also show that, whereas most wild-type V(H)12-expressing B cells are CD5(+), the majority of the splenic V(H)12-expressing BLNK-/- B cells are CD5(-), A small population of V(H)12-expressing, BLNK-/- CD5(+) B cells is detectable in the peritoneal cavity of younger but not older mice, This suggests that BLNK deficiency affects not only the generation but also the persistence of B-1 cells.