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Blood, 1 October 2005, Vol. 106, No. 7, pp. 2318-2328.
Prepublished online as a Blood First Edition Paper on June 16, 2005; DOI 10.1182/blood-2005-02-0557.
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Submitted February 9, 2005
Accepted June 1, 2005
SCL/TAL1 expression level regulates human hematopoietic stem cell self-renewal and engraftment
Damien Reynaud, Emmanuel Ravet, Monique Titeux, Frederic Mazurier, Laurent Renia, Anne Dubart-Kupperschmitt, Paul-Henri Romeo, and Francoise Pflumio*
Department of Hematology, Institut Cochin, U567 INSERM, CNRS UMR 8104, Paris, France
INSERM E0217, Universite V Segalen, Paris, France
Department of Immunology, Institut Cochin, INSERM U567, Bordeaux, France
* Corresponding author; email: plume{at}cochin.inserm.fr.
The fate of hematopoietic stem cells (HSC) is regulated through a combinatorial action of proteins that determine their self-renewal and/or their commitment to differentiation. SCL/TAL1, a bHLH transcription factor, plays key roles in controlling the development of primitive and definitive hematopoiesis during mouse development but its function in adult HSC is still a matter of debate. We report here that the lentiviral mediated enforced expression of TAL1 in human CD34+ cells marginally affects in vitro the differentiation of committed progenitors whereas in vivo the repopulation capacity of the long term scid-repopulating cells (LT-SRC) is enhanced. As a consequence, the production of SRC-derived multipotent progenitors as well as erythroid and myeloid differentiated cells is increased. Looking at the lymphoid compartment, constitutive TAL1 enforced expression impairs B but not T cell differentiation. Expression of a mutant TAL1 protein that cannot bind DNA specifically impairs human LT-SRC amplification indicating a DNA-binding dependent effect of TAL1 on primitive cell populations. These results indicates that TAL1 expression level regulates immature human hematopoietic cells self-renewal and that this regulation requires TAL1 DNA binding activity.
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