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Blood, 1 May 2008, Vol. 111, No. 9, pp. 4500-4510. Prepublished online as a Blood First Edition Paper on February 12, 2008; DOI 10.1182/blood-2007-09-110569. This Article Full Text Full Text (PDF) Supplemental Table and Figures All Versions of this Article: blood-2007-09-110569v1 111/9/4500    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 Google Scholar Articles by Sumanas, S. Articles by Lin, S. PubMed PubMed Citation Articles by Sumanas, S. Articles by Lin, S. Related Collections Hematopoiesis Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMATOPOIESIS AND STEM CELLS Interplay among Etsrp/ER71, Scl, and Alk8 signaling controls endothelial and myeloid cell formation Saulius Sumanas1,2, Gustavo Gomez1, Yan Zhao1, Changwon Park3, Kyunghee Choi3,4, and Shuo Lin1 1 Department of Molecular, Cell and Developmental Biology, University of California, Los Angeles; 2 Division of Developmental Biology, Cincinnati Children's Hospital Medical Center, OH; and 3 Department of Pathology and Immunology and 4 Molecular Cell Biology Program, Washington University School of Medicine, St Louis, MO Vascular endothelial and myeloid cells have been proposed to originate from a common precursor cell, the hemangioblast. The mechanism of endothelial and myeloid cell specification and differentiation is poorly understood. We have previously described the endothelial-specific zebrafish Ets1-related protein (Etsrp), which was both necessary and sufficient to initiate vasculogenesis in the zebrafish embryos. Here we identify human Etv2/ER71 and mouse ER71 proteins as functional orthologs of Etsrp. Overexpression of mouse ER71 and Etsrp caused strong expansion of hemangioblast and vascular endothelial lineages in a zebrafish embryo. In addition, we show that etsrp is also required for the formation of myeloid but not erythroid cells. In the absence of etsrp function, the number of granulocytes and macrophages is greatly reduced. Etsrp overexpression causes expansion of both myeloid and vascular endothelial lineages. Analysis of mosaic embryos indicates that etsrp functions cell autonomously in inducing myeloid lineage. We further demonstrate that the choice of endothelial versus myeloid fate depends on a combinatorial effect of etsrp, scl, and alk8 genes. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

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