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This Article Full Text Full Text (PDF) 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 Vyas, P. Articles by Shivdasani, R. A. Search for Related Content PubMed PubMed Citation Articles by Vyas, P. Articles by Shivdasani, R. A. Related Collections Hematopoiesis and Stem Cells Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, Vol. 93 No. 9 (May 1), 1999: pp. 2867-2875 Consequences of GATA-1 Deficiency in Megakaryocytes and Platelets Paresh Vyas, Kenneth Ault, Carl W. Jackson, Stuart H. Orkin, and Ramesh A. Shivdasani From the Department of Hematology-Oncology and Howard Hughes Medical Institute, Children's Hospital, Boston; the Departments of Adult Oncology and Medicine, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA; Maine Medical Center Research Institute, South Portland, ME; and the Department of Experimental Hematology, St Jude Children's Research Hospital, Memphis, TN. In the absence of the hematopoietic transcription factor GATA-1, mice develop thrombocytopenia and an increased number of megakaryocytes characterized by marked ultrastructural abnormalities. These observations establish a critical role for GATA-1 in megakaryopoiesis and raise the question as to how GATA-1 influences megakaryocyte maturation and platelet production. To begin to address this, we have performed a more detailed examination of the megakaryocytes and platelets produced in mice that lack GATA-1 in this lineage. Our analysis demonstrates that compared with their normal counterparts, GATA-1-deficient primary megakaryocytes exhibit significant hyperproliferation in liquid culture, suggesting that the megakaryocytosis seen in animals is nonreactive. Morphologically, these mutant megakaryocytes are small and show evidence of retarded nuclear and cytoplasmic development. A significant proportion of these cells do not undergo endomitosis and express markedly lower levels of mRNA of all megakaryocyte-associated genes tested, including GPIb, GPIb, platelet factor 4 (PF4), c-mpl, and p45 NF-E2. These results are consistent with regulation of a program of megakaryocytic differentiation by GATA-1. Bleeding times are significantly prolonged in mutant animals. GATA-1-deficient platelets show abnormal ultrastructure, reminiscent of the megakaryocytes from which they are derived, and exhibit modest but selective defects in platelet activation in response to thrombin or to the combination of adenosine diphosphate (ADP) and epinephrine. Our findings indicate that GATA-1 serves multiple functions in megakaryocyte development, influencing both cellular growth and maturation. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J. W. Snow and S. H. Orkin Translational Isoforms of FOG1 Regulate GATA1-interacting Complexes J. Biol. Chem., October 23, 2009; 284(43): 29310 - 29319. [Abstract] [Full Text] [PDF] Z. Huang, L. C. Dore, Z. Li, S. H. Orkin, G. Feng, S. Lin, and J. D. Crispino GATA-2 Reinforces Megakaryocyte Development in the Absence of GATA-1 Mol. Cell. Biol., September 15, 2009; 29(18): 5168 - 5180. [Abstract] [Full Text] [PDF] A. R. Migliaccio, F. Martelli, M. 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