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Blood, 1 November 2007, Vol. 110, No. 9, pp. 3417-3425. Prepublished online as a Blood First Edition Paper on August 3, 2007; DOI 10.1182/blood-2006-11-057307. This Article Full Text (PDF) All Versions of this Article: blood-2006-11-057307v1 110/9/3417    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 Basu, P. Articles by Lloyd, J. A. Search for Related Content PubMed PubMed Citation Articles by Basu, P. Articles by Lloyd, J. A. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted November 9, 2006 Accepted July 23, 2007 EKLF and KLF2 have compensatory roles in embryonic -globin gene expression and primitive erythropoiesis Priyadarshi Basu, Tina K. Lung, Wafaa Lemsaddek, Thanh Giang Sargent, David C. Williams Jr., Mohua Basu, Latasha C. Redmond, Jerry B Lingrel, Jack L. Haar, and Joyce A. Lloyd* Department of Human Genetics, Virginia Commonwealth University, Richmond, VA, United States Department of Anatomy and Neurobiology, Virginia Commonwealth University, Richmond, VA, United States Department of Pathology, Virginia Commonwealth University, Richmond, VA, United States Dept of Molecular Genetics, Biochemistry, and Microbiology, College of Medicine, University of Cincinnati, Cincinnati, OH, United States Massey Cancer Center, Virginia Commonwealth University, Richmond, VA, United States * Corresponding author; email: jlloyd{at}vcu.edu. The Kruppel-like C2/H2 zinc finger transcription factors (KLFs) control development and differentiation. Erythroid Kruppel-like Factor (EKLF or KLF1) regulates adult -globin gene expression, and is necessary for normal definitive erythropoiesis. KLF2 is required for normal embryonic Ey- and h1-, but not adult –globin, gene expression in mice. Both EKLF and KLF2 play roles in primitive erythroid cell development. To investigate potential interactions between these genes, EKLF/KLF2 double mutant embryos were analyzed. EKLF-/-KLF2-/- mice appear anemic at embryonic day 10.5 (E10.5) and die before E11.5, whereas single knockout EKLF-/- or KLF2-/- embryos are grossly normal at E10.5 and die later than EKLF-/-KLF2-/- embryos. At E10.5, Ey- and h1-globin mRNA is greatly reduced in EKLF-/-KLF2-/-, compared to EKLF-/- or KLF2-/- embryos, consistent with the observed anemia. Light and electron microscopic analyses of E9.5 EKLF-/-KLF2-/- yolk sacs, and cytospins, indicate that erythroid and endothelial cells are morphologically more abnormal than in either single knockout. EKLF-/-KLF2-/- erythroid cells are markedly irregularly shaped, suggesting membrane abnormalities. EKLF and KLF2 may have coordinate roles in a common progenitor to erythroid and endothelial cells. The data indicate that EKLF and KLF2 have redundant functions in embryonic -like globin gene expression, primitive erythropoiesis, and endothelial development. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: F. Marques-Garcia, N. Ferrandiz, R. Fernandez-Alonso, L. Gonzalez-Cano, M. Herreros-Villanueva, M. Rosa-Garrido, B. Fernandez-Garcia, J. P. Vaque, M. M. Marques, M. E. Alonso, et al. p73 Plays a Role in Erythroid Differentiation through GATA1 Induction J. Biol. Chem., August 7, 2009; 284(32): 21139 - 21156. [Abstract] [Full Text] [PDF] Y.-F. Fu, T.-T. Du, M. Dong, K.-Y. Zhu, C.-B. Jing, Y. Zhang, L. Wang, H.-B. Fan, Y. Chen, Y. Jin, et al. Mir-144 selectively regulates embryonic {alpha}-hemoglobin synthesis during primitive erythropoiesis Blood, February 5, 2009; 113(6): 1340 - 1349. [Abstract] [Full Text] [PDF]

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