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Blood, 15 September 2007, Vol. 110, No. 6, pp. 1814-1823.
Prepublished online as a Blood First Edition Paper on May 29, 2007; DOI 10.1182/blood-2007-02-075648.
 Previous Article | Next Article 
Submitted February 21, 2007
Accepted May 23, 2007
The hedgehog receptor patched
controls lymphoid lineage commitment
Anja Uhmann, Kai Dittmann, Frauke Nitzki, Ralf Dressel, Milena Koleva, Anke Frommhold, Arne Zibat, Claudia Binder, Ibrahim Adham, Mirko Nitsche, Tanja Heller, Victor Armstrong, Walter Schulz-Schaeffer, Jurgen Wienands, and Heidi Hahn*
Institute of Human Genetics, University Goettingen, Goettingen, Germany
Department of Cellular and Molecular Immunology, University Goettingen, Goettingen, Germany
Department of Haematology and Oncology, University Goettingen, Goettingen, Germany
Department of Radiation Therapy and Oncology, University Goettingen, Goettingen, Germany
Department of Clinical Chemistry, University Goettingen, Goettingen, Germany
Department of Neuropathology, University Goettingen, Goettingen, Germany
* Corresponding author; email: hhahn{at}gwdg.de.
A first step in hematopoiesis is the specification of the lymphoid and myeloid lineages from multipotent progenitor cells in the bone marrow. Using a conditional ablation strategy in adult mice, we show that this differentiation step requires Patched (Ptch), the cell surface-bound receptor for Hedgehog (Hh). In the absence of Ptch, the development of T and B lymphoid lineages are blocked at the level of the common lymphoid progenitor in the bone marrow. Consequently, the generation of peripheral T and B cells is abrogated. Cells of the myeloid lineage develop normally in Ptch mutant mice. Finally, adoptive transfer experiments identified the stromal cell compartment as a critical Ptch-dependent inducer of lymphoid versus myeloid lineage commitment. Our data show that Ptch acts as a master switch for proper diversification of hematopoietic stem cells in the adult organism.
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