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Tal1 Transgenic Expression Reveals Absence of B Lymphocytes

Comprehensive Cancer Center, Human Cancer Genetics Program and Department of Molecular Virology, Immunology, and Medical Genetics, OSU School of Medicine, Ohio State University, Columbus, Ohio

Requests for reprints: Yuri Pekarsky, Comprehensive Cancer Center, Ohio State University, 435 Wiseman Hall, 410 West 12th Avenue, Columbus, OH 43210. Phone: 614-292-3120; Fax: 614-292-3312; E-mail: Pekarsky.Yuri{at}osumc.edu.

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 Eµ-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 Eµ-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)