| First Author | Palamarchuk A | Year | 2006 |
| Journal | Cancer Res | Volume | 66 |
| Issue | 12 | Pages | 6014-7 |
| PubMed ID | 16778172 | Mgi Jnum | J:110108 |
| Mgi Id | MGI:3639375 | Doi | 10.1158/0008-5472.CAN-06-0937 |
| Citation | Palamarchuk A, et al. (2006) Tal1 transgenic expression reveals absence of B lymphocytes. Cancer Res 66(12):6014-7 |
| abstractText | TAL1 oncogene encodes a helix-loop-helix transcription factor, Tal1, which is required for blood cell development, and its activation is a frequent event in T-cell acute lymphoblastic leukemia. Tal1 interacts and inhibits other helix-loop-helix factors such as E47 and HEB. To investigate the function of Tal1 in B cells, we generated Emu-TAL1 transgenic mouse line, expressing Tal1 in mouse B-cell lineage. Fluorescence-activated cell sorting (FACS) analysis of lymphocytes isolated from spleens of five out of five founders reveals complete absence of IgM- or CD19-expressing cells. Only 2% to 3% of these cells were B220+ and 100% of B220+ cells were CD43+, indicating that these mice were able to make pro-B cells. Similarly, FACS analysis of bone marrow cells in Emu-TAL1 mice revealed complete absence of B220+IgM+ and B220+CD19+ cells. Analysis of the recombination status of IgH genes revealed the presence of D-J but absence or drastic reduction of V-D-J rearrangements. Our results suggest that Tal1 overexpression in B cells results in a phenotype similar to that of B cells of E47/E2A knockout animals. This represents first in vivo evidence that Tal1 can completely inhibit E47/E2A function. |
