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Blood, 1 November 2006, Vol. 108, No. 9, pp. 2989-2997. Prepublished online as a Blood First Edition Paper on July 11, 2006; DOI 10.1182/blood-2006-05-022137. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2006-05-022137v1 108/9/2989    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 HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Schmerer, M. Articles by Evans, T. Search for Related Content PubMed PubMed Citation Articles by Schmerer, M. Articles by Evans, T. Related Collections Hematopoiesis and Stem Cells Signal Transduction Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMATOPOIESIS STAT5 acts as a repressor to regulate early embryonic erythropoiesis Matthew Schmerer, Ingrid Torregroza, Aude Pascal, Muriel Umbhauer, and Todd Evans From the Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, NY; and the Laboratoire de Biologie du développement, Centre National de la Recherche Scientifique/Université Pierre et Marie Curie, Equipe Signalisation et Morphogénèse, Paris, France. STAT5 regulates definitive (adult stage) erythropoiesis through its ability to transduce signals from the erythropoietin receptor. A function for STAT-dependent signaling during primitive (embryonic) erythropoiesis has not been analyzed. We tested this in the Xenopus system, because STAT5 is expressed at the right time and place to regulate development of the embryonic primitive ventral blood island. Depletion of STAT5 activity results in delayed accumulation of the first globinexpressing cells, indicating that the gene does regulate primitive erythropoiesis. Our results suggest that in this context STAT5 functions as a repressor, since forced expression of an activator isoform blocks erythropoiesis, while embryos expressing a repressor isoform develop normally. The erythroid phenotype caused by the activator isoform of STAT5 resembles that caused by overexpression of fibroblast growth factor (FGF). We show that STAT5 isoforms can function epistatic to FGF and can be phosphorylated in response to hyperactivated FGF signaling in Xenopus embryos. Therefore, our data indicate that STAT5 functions in both primitive and definitive erythropoiesis, but by different mechanisms. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J. Zhang and P. A. Ney EPOR signaling: 450 million years' history Blood, October 1, 2007; 110(7): 2225 - 2226. [Full Text] [PDF] C. Schindler, D. E. Levy, and T. Decker JAK-STAT Signaling: From Interferons to Cytokines J. Biol. Chem., July 13, 2007; 282(28): 20059 - 20063. [Full Text] [PDF]

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