Tal1 Transgenic Expression Reveals Absence of B Lymphocytes

Alexey Palamarchuk, Nicola Zanesi, Rami I. Aqeilan, Alexey Efanov, Vadim Maximov, Urmila Santanam, John P. Hagan, Carlo M. Croce, Yuri Pekarsky
2006 Cancer Research  
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 EM-TAL1 transgenic mouse line, expressing Tal1 in mouse B-cell lineage. Fluorescence-activated cell sorting (FACS) analysis of lymphocytes isolated from spleens of
more » ... ive 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 EM-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. (Cancer Res 2006; 66(12): 6014-7) Requests for reprints: Yuri Pekarsky,
doi:10.1158/0008-5472.can-06-0937 pmid:16778172 fatcat:geob7jaifvgcvaerxi24kn6qii