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Blood, 15 April 2008, Vol. 111, No. 8, pp. 4375-4385. Prepublished online as a Blood First Edition Paper on February 7, 2008; DOI 10.1182/blood-2007-09-115121. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2007-09-115121v1 111/8/4375    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Gutiérrez, L. Articles by Ohneda, K. Search for Related Content PubMed PubMed Citation Articles by Gutiérrez, L. Articles by Ohneda, K. Related Collections Hematopoiesis and Stem Cells Red Cells Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  RED CELLS Ablation of Gata1 in adult mice results in aplastic crisis, revealing its essential role in steady-state and stress erythropoiesis Laura Gutiérrez1,*, Saho Tsukamoto2,*, Mikiko Suzuki2,*, Harumi Yamamoto-Mukai2, Masayuki Yamamoto2,3, Sjaak Philipsen1, and Kinuko Ohneda4 1 Department of Cell Biology, Erasmus Medical College, Rotterdam, The Netherlands; 2 Graduate School of Comprehensive Human Sciences, Center for Tsukuba Advanced Research Alliance, and Environmental Response Project, Exploratory Research for Advanced Technology, Japan Science and Technology Corporation, University of Tsukuba, Tsukuba, Japan; 3 Department of Medical Biochemistry, Tohoku University Graduate School of Medicine, Sendai, Japan; and 4 Department of Pharmacy, Faculty of Pharmacy, Takasaki University of Health and Welfare, Takasaki, Japan The transcription factor Gata1 is expressed in several hematopoietic lineages and plays essential roles in normal hematopoietic development during embryonic stages. The lethality of Gata1-null embryos has precluded determination of its role in adult erythropoiesis. Here we have examined the effects of Gata1 loss in adult erythropoiesis using conditional Gata1 knockout mice expressing either interferon- or tamoxifen-inducible Cre recombinase (Mx-Cre and Tx-Cre, respectively). Mx-Cre–mediated Gata1 recombination, although incomplete, resulted in maturation arrest of Gata1-null erythroid cells at the proerythroblast stage, thrombocytopenia, and excessive proliferation of megakaryocytes in the spleen. Tx-Cre–mediated Gata1 recombination resulted in depletion of the erythroid compartment in bone marrow and spleen. Formation of the early and late erythroid progenitors in bone marrow was significantly reduced in the absence of Gata1. Furthermore, on treatment with a hemolytic agent, these mice failed to activate a stress erythropoietic response, despite the rising erythropoietin levels. These results indicate that, in addition to the requirement of Gata1 in adult megakaryopoiesis, Gata1 is necessary for steady-state erythropoiesis and for erythroid expansion in response to anemia. Thus, ablation of Gata1 in adult mice results in a condition resembling aplastic crisis in human. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

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