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Blood, 1 December 2004, Vol. 104, No. 12, pp. 3558-3564.
Prepublished online as a Blood First Edition Paper on July 22, 2004; DOI 10.1182/blood-2004-04-1535.
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HEMATOPOIESIS
The transcriptionally active form of AML1 is required for hematopoietic rescue of the AML1-deficient embryonic para-aortic splanchnopleural (P-Sp) region
Susumu Goyama,
Yuko Yamaguchi,
Yoichi Imai,
Masahito Kawazu,
Masahiro Nakagawa,
Takashi Asai,
Keiki Kumano,
Kinuko Mitani,
Seishi Ogawa,
Shigeru Chiba,
Mineo Kurokawa, and
Hisamaru Hirai
From the Departments of Hematology/Oncology and Regeneration Medicine for Hematopoiesis, Graduate School of Medicine, University of Tokyo, Tokyo, Japan; Department of Cell Therapy/Transplantation Medicine, University of Tokyo Hospital, University of Tokyo, Tokyo, Japan; and Department of Hematology, Dokkyo University School of Medicine, Tochigi, Japan.
Acute myelogenous leukemia 1 (AML1; runt-related transcription factor 1 [Runx1]) is a member of Runx transcription factors and is essential for definitive hematopoiesis. Although AML1 possesses several subdomains of defined biochemical functions, the physiologic relevance of each subdomain to hematopoietic development has been poorly understood. Recently, the consequence of carboxy-terminal truncation in AML1 was analyzed by the hematopoietic rescue assay of AML1-deficient mouse embryonic stem cells using the gene knock-in approach. Nonetheless, a role for specific internal domains, as well as for mutations found in a human disease, of AML1 remains to be elucidated. In this study, we established an experimental system to efficiently evaluate the hematopoietic potential of AML1 using a coculture system of the murine embryonic para-aortic splanchnopleural (P-Sp) region with a stromal cell line, OP9. In this system, the hematopoietic defect of AML1-deficient P-Sp can be rescued by expressing AML1 with retroviral infection. By analysis of AML1 mutants, we demonstrated that the hematopoietic potential of AML1 was closely related to its transcriptional activity. Furthermore, we showed that other Runx transcription factors, Runx2/AML3 or Runx3/AML2, could rescue the hematopoietic defect of AML1-deficient P-Sp. Thus, this experimental system will become a valuable tool to analyze the physiologic function and domain contribution of Runx proteins in hematopoiesis.
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