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 Blood, 19 February 2009, Vol. 113, No. 8, pp. 1661-1669.
Prepublished online as a Blood First Edition Paper on October 31, 2008; DOI 10.1182/blood-2008-01-135012.

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HEMATOPOIESIS AND STEM CELLS

Menin regulates the function of hematopoietic stem cells and lymphoid progenitors

Ivan Maillard15, Ya-Xiong Chen5,6, Ann Friedman1, Yuqing Yang5,6, Anthony T. Tubbs5,6, Olga Shestova5,7, Warren S. Pear5,6,8, and Xianxin Hua5,6

1 Center for Stem Cell Biology, Life Sciences Institute, 2 Division of Hematology-Oncology, Department of Internal Medicine, and 3 Department of Cell and Developmental Biology, University of Michigan, Ann Arbor; and 4 Division of Hematology-Oncology, 5 Abramson Family Cancer Research Institute, 6 Department of Cancer Biology, 7 Department of Pathology and Laboratory Medicine, and 8 Institute of Medicine and Engineering, University of Pennsylvania, Philadelphia

Men1 is a tumor suppressor gene mutated in endocrine neoplasms. Besides its endocrine role, the Men1 gene product menin interacts with the mixed lineage leukemia (MLL) protein, a histone H3 lysine 4 methyltransferase. Although menin and MLL fusion proteins cooperate to activate Homeobox (Hox) gene expression during transformation, little is known about the normal hematopoietic functions of menin. Here, we studied hematopoiesis after Men1 ablation. Menin loss modestly impaired blood neutrophil, lymphocyte, and platelet counts. Without hematopoietic stress, multilineage and myelo-erythroid bone marrow progenitor numbers were preserved, while B lymphoid progenitors were decreased. In contrast, competitive transplantation revealed a marked functional defect of long-term hematopoietic stem cells (HSC) in the absence of menin, despite normal initial homing of progenitors to the bone marrow. HoxA9 gene expression was only modestly decreased in menin-deficient HSCs. These observations reveal a novel and essential role for menin in HSC homeostasis that was most apparent during situations of hematopoietic recovery, suggesting that menin regulates molecular pathways that are essential during the adaptive HSC response to stress.


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HOXA9 Modulates Its Oncogenic Partner Meis1 To Influence Normal Hematopoiesis
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