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Blood, 15 November 2006, Vol. 108, No. 10, pp. 3329-3334.
Prepublished online as a Blood First Edition Paper on August 3, 2006; DOI 10.1182/blood-2006-04-019570.
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HEMATOPOIESIS
AML1/Runx1 rescues Notch1-null mutation-induced deficiency of para-aortic splanchnopleural hematopoiesis
Masahiro Nakagawa,
Motoshi Ichikawa,
Keiki Kumano,
Susumu Goyama,
Masahito Kawazu,
Takashi Asai,
Seishi Ogawa,
Mineo Kurokawa, and
Shigeru Chiba
From the Departments of Hematology and Oncology and Regeneration Medicine for Hematopoiesis, Graduate School of Medicine, University of Tokyo, Japan; and the Department of Cell Therapy and Transplantation Medicine, University of Tokyo Hospital, Tokyo, Japan.
The Notch1-RBP-J and the transcription factor Runx1 pathways have been independently shown to be indispensable for the establishment of definitive hematopoiesis. Importantly, expression of Runx1 is down-regulated in the para-aortic splanchnopleural (P-Sp) region of Notch1- and Rbpsuh-null mice. Here we demonstrate that Notch1 up-regulates Runx1 expression and that the defective hematopoietic potential of Notch1-null P-Sp cells is successfully rescued in the OP9 culture system by retroviral transfer of Runx1. We also show that Hes1, a known effector of Notch signaling, potentiates Runx1-mediated transactivation. Together with the recent findings in zebrafish, Runx1 is postulated to be a cardinal down-stream mediator of Notch signaling in hematopoietic development throughout vertebrates. Our findings also suggest that Notch signaling may modulate both expression and transcriptional activity of Runx1.
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