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Blood, 15 July 2002, Vol. 100, No. 2, pp. 491-500
HEMATOPOIESIS
Ectopic expression of TAL-1 protein in Ly-6E.1-htal-1
transgenic mice induces defects in B- and T-lymphoid
differentiation
Nicolas Goardon,
Annette Schuh,
Iman Hajar,
Xiaoqian Ma,
Hélène Jouault,
Elaine Dzierzak,
Paul-Henri Roméo, and
Leïla Maouche-Chrétien
From the Institut Cochin, Département
d'Hématologie, INSERM, CNRS, Paris, France; the Department of
Cell Biology and Genetics, Erasmus University, Rotterdam, The
Netherlands; and the Département d'Hématologie,
Hôpital Henri Mondor, Créteil, France.
The tal-1 gene encodes a basic helix-loop-helix (bHLH)
transcription factor required for primitive and definitive
hematopoiesis. Additionally, ectopic activation of the
tal-1 gene during T lymphopoiesis occurs in numerous cases
of human T-cell acute lymphoblastic leukemia. With the use of
transgenic mice, we show that, in adult hematopoiesis, constitutive
expression of TAL-1 protein causes disorders in the hematopoietic
lineages that normally switch off tal-1 gene expression during their differentiation process. Myelopoiesis was characterized by
a moderate increase of myeloid precursors and by Sca-1 antigen persistence. Although no lymphoid leukemia was observed, T
lymphopoiesis and B lymphopoiesis were severely impaired. Transgenic
mice showed reduced thymic cellularity together with a decrease in
double-positive cells and a concurrent increase in the single-positive
population. B cells exhibited a differentiation defect characterized by
a reduction of the B-cell compartment most likely because of a
differentiation block upstream of the intermediate pro-B progenitor. B
cells escaping this defect developed normally, but transgenic
splenocytes presented a defect in immunoglobulin class switch
recombination. Altogether, these results enlighten the fine-tuning of
TAL-1 expression during adult hematopoiesis and indicate why TAL-1
expression has to be switched off in the lymphoid lineages.
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