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Prepublished online as a Blood First Edition Paper on April 3, 2003; DOI 10.1182/blood-2002-06-1848.
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Blood, 1 August 2003, Vol. 102, No. 3, pp. 858-866
HEMATOPOIESIS
Impaired hematopoiesis in mice lacking the transcription factor Sp3
Pieter Fokko van Loo,
Peter Bouwman,
Kam-Wing Ling,
Sabine Middendorp,
Guntram Suske,
Frank Grosveld,
Elaine Dzierzak,
Sjaak Philipsen, and
Rudolf W. Hendriks
From the Department of Cell Biology and the Department of Immunology, Erasmus MC, Rotterdam, The Netherlands; and the Institut für Molekularbiologie und Tumorforschung Philipps-Universität Marburg, Germany
As the zinc-finger transcription factor specificity protein 3 (Sp3) has been implicated in the regulation of many hematopoietic-specific genes, we analyzed the role of Sp3 in hematopoiesis. At embryonic day 18.5 (E18.5), Sp3-/- mice exhibit a partial arrest of T-cell development in the thymus and B-cell numbers are reduced in liver and spleen. However, pre–B-cell proliferation and differentiation into immunoglobulin M–positive (IgM+) B cells in vitro are not affected. At E14.5 and E16.5, Sp3-/- mice exhibit a significant delay in the appearance of definitive erythrocytes in the blood, paralleled by a defect in the progression of differentiation of definitive erythroid cells in vitro. Perinatal death of the null mutants precludes the analysis of adult hematopoiesis in Sp3-/- mice. We therefore investigated the ability of E12.5 Sp3-/- liver cells to contribute to the hematopoietic compartment in an in vivo transplantation assay. Sp3-/- cells were able to repopulate the B- and T-lymphoid compartment, albeit with reduced efficiency. In contrast, Sp3-/- cells showed no significant engraftment in the erythroid and myeloid lineages. Thus, the absence of Sp3 results in cell-autonomous hematopoietic defects, affecting in particular the erythroid and myeloid cell lineages.
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