| First Author | Nutt SL | Year | 1997 |
| Journal | Immunobiology | Volume | 198 |
| Issue | 1-3 | Pages | 227-35 |
| PubMed ID | 9442394 | Mgi Jnum | J:45254 |
| Mgi Id | MGI:1194700 | Doi | 10.1016/S0171-2985(97)80043-5 |
| Citation | Nutt SL, et al. (1997) Essential functions of Pax-5 (BSAP) in pro-B cell development. Immunobiology 198(1-3):227-35 |
| abstractText | Pax-5 codes for the transcription factor BSAP which is expressed in all B-lymphoid tissues in addition to the developing central nervous system and testis. Within the B-lymphoid lineage, Pax-5 expression is already detected in the earliest B cell progenitors and persists up to the mature B cell stage. Targeted inactivation of the Pax-5 gene in the mouse germline revealed a differential dependency of fetal and adult B- lymphopoiesis on this transcription factor. Pax-5 is required for the differentiation of the earliest B-lineage-committed precursor cells in the fetal liver. In contrast, B cell development in the adult bone marrow progresses up to an early pro-B cell stage in the absence of Pax-5 function. The expression of CD19, Ig alpha (mb-1) and N-myc is severely reduced in Pax-5-deficient pro-B cells. These BSAP target genes are, however, unlikely to explain the early developmental block based on their known function in B cell development. Moreover, VH-to-DHJH rearrangements at the immunoglobulin heavy-chain locus are approximately 50-fold reduced in Pax-5-deficient pro B-cells, while the DH-to-JH rearrangements occur at a normal frequency. However, the expression of rearranged mu heavy-chain transgenes does not allow Pax-5-deficient pro-B cells to develop further to the pre-B cell stage. Together these data demonstrate therefore that B cell development in the Pax-5 deficient bone marrow is arrested at an early pro-B cell stage which is not yet responsive to pre-B cell receptor signaling. |
