SEARCH:   Advanced

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 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 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 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. Related Collections Hematopoiesis and Stem Cells Gene Expression Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMATOPOIESIS 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. Scott Swindle, Claudiu V. Cotta, Larry Gartland, Edward W. Scott, and Christopher A. Klug From the Department of Microbiology and Division of Developmental and Clinical Immunology, the Department of Human Genetics, and the Department of Pathology, University of Alabama Birmingham, AL; Department of Molecular Genetics and Microbiology, University of Florida at Gainesville, Gainesville, FL. 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 macrophages. 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 HSCs, PU.1-/- embryos were analyzed at various stages of embryonic development. The absolute number and frequency of HSCs 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 progenitors (CMPs) and granulocyte-macrophage progenitors (GMPs) but retained megakaryocyteerythroid progenitors (MEPs). Consistent with the loss of HSC activity, a 10-fold reduction in erythroid progenitors (mature erythroid burst-forming units [BFUEs]) 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. (Blood. 2004;104:3894-3900) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: 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. Speck T-lymphoid, megakaryocyte, and granulocyte development are sensitive to decreases in CBF{beta} dosage. Blood, January 1, 2007; 109(1): 11 - 21. [Abstract] [Full Text] [PDF] T. Katsumoto, Y. Aikawa, A. Iwama, S. Ueda, H. Ichikawa, T. Ochiya, and I. Kitabayashi MOZ is essential for maintenance of hematopoietic stem cells. Genes & Dev., May 15, 2006; 20(10): 1321 - 1330. [Abstract] [Full Text] [PDF] M. D. Liang, Y. Zhang, D. McDevit, S. Marecki, and B. S. Nikolajczyk The Interleukin-1beta Gene Is Transcribed from a Poised Promoter Architecture in Monocytes J. Biol. Chem., April 7, 2006; 281(14): 9227 - 9237. [Abstract] [Full Text] [PDF] M. Ye, O. Ermakova, and T. Graf PU.1 is not strictly required for B cell development and its absence induces a B-2 to B-1 cell switch J. Exp. Med., November 21, 2005; 202(10): 1411 - 1422. [Abstract] [Full Text] [PDF] K. Maki, T. Yamagata, T. Asai, I. Yamazaki, H. Oda, H. Hirai, and K. Mitani Dysplastic definitive hematopoiesis in AML1/EVI1 knock-in embryos Blood, September 15, 2005; 106(6): 2147 - 2155. [Abstract] [Full Text] [PDF] F. Rosenbauer, S. Koschmieder, U. Steidl, and D. G. Tenen Effect of transcription-factor concentrations on leukemic stem cells Blood, September 1, 2005; 106(5): 1519 - 1524. [Abstract] [Full Text] [PDF] H. Iwasaki, C. Somoza, H. Shigematsu, E. A. Duprez, J. Iwasaki-Arai, S.-i. Mizuno, Y. Arinobu, K. Geary, P. Zhang, T. Dayaram, et al. Distinctive and indispensable roles of PU.1 in maintenance of hematopoietic stem cells and their differentiation Blood, September 1, 2005; 106(5): 1590 - 1600. [Abstract] [Full Text] [PDF]

	Copyright © 2004 by American Society of Hematology         Online ISSN: 1528-0020