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Blood, 15 December 2004, Vol. 104, No. 13, pp. 3894-3900. Prepublished online as a Blood First Edition Paper on August 24, 2004; DOI 10.1182/blood-2002-08-2425. This Article Full Text (PDF) All Versions of this Article: 2002-08-2425v1 104/13/3894    most recent Alert me when this article is cited Alert me if a correction is posted 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 Kim, H.-G. Articles by Klug, C. A Search for Related Content PubMed PubMed Citation Articles by Kim, H.-G. Articles by Klug, C. A Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted August 7, 2002 Accepted July 12, 2004 The ETS-family transcription factor, PU.1, is necessary for the maintenance of fetal liver hematopoietic stem cells Hyung-Gyoon Kim, Cristina G de Guzman, C S Swindle, Claudiu V Cotta, Larry Gartland, Edward W Scott, and Christopher A Klug* Department of Microbiology and Division of Developmental and Clinical Immunology, University of Alabama, Birmingham, AL, USA Department of Human Genetics, University of Alabama, Birmingham, AL, USA Department of Pathology, University of Alabama, Birmingham, AL, USA Department of Molecular Genetics and Microbiology, University of Florida, Gainesville, FL, USA * Corresponding author; email: chrisk{at}uab.edu. PU.1 is a member of the ETS family of transcription factors and is required for the development of multiple hematopoietic lineages. PU.1-/- mice die from hematopoietic failure at about embryonic day 18.5 (e18.5) and show a complete absence of B cells, mature T cells and macrophage. This phenotype suggests that PU.1 may function at the level of the hematopoietic stem cell (HSC) or a multilineage progenitor. To investigate the role of PU.1 in the regulation of HSC, PU.1-/- embryos were analyzed at various stages of embryonic development. The absolute number and frequency of HSC were determined by flow cytometric analysis of c-Kit+Thy-1.1loLin-Sca-1+(KTLS) cells. We found that KTLS cells were absent or severely reduced in PU.1-/- fetal liver from e12.5 to e15.5. Progenitor cells with a c-Kit+Lin-AA4.1+ and c-Kit+Lin-CD34+ phenotype were also severely reduced. In addition, PU.1-/- fetal liver at e14.5 lacked common myeloid and granulocyte-macrophage progenitors (CMP and GMP) but retained megakaryocyte-erythroid progenitors (MEP). Consistent with the loss of HSC activity, a 10-fold reduction in erythroid progenitors (mature BFU-E) was observed between e14.5 and e16.5. These data suggest that PU.1 plays an important role in the maintenance or expansion of HSC number in murine fetal liver. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: B.P. Levi and S.J. Morrison Stem Cells Use Distinct Self-renewal Programs at Different Ages Cold Spring Harb Symp Quant Biol, January 15, 2009; (2009) sqb.2008.73.049v1. [Abstract] [PDF] P. Rimmele, O. Kosmider, P. Mayeux, F. Moreau-Gachelin, and C. Guillouf Spi-1/PU.1 participates in erythroleukemogenesis by inhibiting apoptosis in cooperation with Epo signaling and by blocking erythroid differentiation Blood, April 1, 2007; 109(7): 3007 - 3014. [Abstract] [Full Text] [PDF] L. Talebian, Z. Li, Y. Guo, J. Gaudet, M. E. Speck, D. Sugiyama, P. Kaur, W. S. Pear, I. Maillard, and N. A. 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