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 Blood, 15 November 2005, Vol. 106, No. 10, pp. 3396-3404.
Prepublished online as a Blood First Edition Paper on August 4, 2005; DOI 10.1182/blood-2005-04-1739.

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HEMATOPOIESIS

MEK kinase 1 activity is required for definitive erythropoiesis in the mouse fetal liver

Barbara Bonnesen, Cathrine Orskov, Susanne Rasmussen, Peter Johannes Holst, Jan Pravsgaard Christensen, Karsten Wessel Eriksen, Klaus Qvortrup, Niels Odum, and Tord Labuda

From the Institute of Molecular Biology and Physiology, Department of Immunology, the Department of Medical Anatomy, the Department of Medical Pharmacology, and the Department of Medical Microbiology and Immunology, University of Copenhagen, Denmark.

Mitogen-activated protein kinase/extracellular signal to regulated kinase (MEK) kinase 1 (MEKK1) is a c-Jun N-terminal kinase (JNK) activating kinase known to be implicated in proinflammatory responses and cell motility. Using mice deficient for MEKK1 kinase activity (Mekk1{Delta}KD) we show a role for MEKK1 in definitive mouse erythropoiesis. Although Mekk1{Delta}KD mice are alive and fertile on a 129 x C57/BL6 background, the frequency of Mekk1{Delta}KD embryos that develop past embryonic day (E) 14.5 is dramatically reduced when backcrossed into the C57/BL6 background. At E13.5, Mekk1{Delta}KD embryos have normal morphology but are anemic due to failure of definitive erythropoiesis. When Mekk1{Delta}KD fetal liver cells were transferred to lethally irradiated wild-type hosts, mature red blood cells were generated from the mutant cells, suggesting that MEKK1 functions in a non–cell-autonomous manner. Based on immunohistochemical and hemoglobin chain transcription analysis, we propose that the failure of definitive erythropoiesis is due to a deficiency in enucleation activity caused by insufficient macrophage-mediated nuclear DNA destruction.


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