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Blood, 15 February 2004, Vol. 103, No. 4, pp. 1278-1285. Prepublished online as a Blood First Edition Paper on October 23, 2003; DOI 10.1182/blood-2003-06-2158. This Article Full Text (PDF) All Versions of this Article: 2003-06-2158v1 103/4/1278    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 Wang, Q. Articles by Dai, W. Search for Related Content PubMed PubMed Citation Articles by Wang, Q. Articles by Dai, W. Social Bookmarking                   What's this? Submitted July 8, 2003 Accepted September 22, 2003 BUBR1-deficiency results in abnormal megakaryopoiesis Qi Wang, Tongyi Liu, Yuqiang Fang, Suqing Xie, Xuan Huang, Radma Mahmood, Gita Ramasiwamy, Kathleen M Sakamoto, Zbigniew Darzynkiewicz, Ming Xu, and Wei Dai* Division of Molecular Carcinogenesis, Department of Medicine, New York Medical College, Valhalla, NY, USA; Brander Cancer Institute, New York Medical College, Valhalla, NY, USA Core Facility for Histopathology, Albert Einstein College of Medicine, Bronx, NY, USA Department of Pathology, New York Medical College, Valhalla, NY, USA Division of Hematology-Oncology, Mattel Children's Hospital, Department of Pathology and Laboratory Medicine, UCLA Jonsson Comprehensive Cancer Center, Molecular Biology Institute, David Geffen School of Medicine, Los Angeles, CA, USA Department of Cell Biology, University of Cincinnati College of Medicine, Cincinnati, OH, USA * Corresponding author; email: wei_dai{at}nymc.edu. The physiological function of BUBR1, a key component of the spindle checkpoint, was examined by the generation of BUBR1 mutant mice. BUBR1-/- embryos failed to survive beyond day 8.5 in utero as a result of extensive apoptosis. Whereas BUBR1+/- blastocysts grew relatively normally in vitro, BUBR1-/- blastocysts exhibited impaired proliferation and atrophied. Adult BUBR1+/- mice manifested splenomegaly and abnormal megakaryopoiesis. BUBR1 haploinsufficiency resulted in an increase in the number of splenic megakaryocytes, which was correlated with an increase in megakaryocytic, but a decrease in erythroid, progenitors in bone marrow cells. RNA interference-mediated down-regulation of BUBR1 also caused an increase in polyploidy formation in murine embryonic fibroblast cells and enhanced megakaryopoiesis in bone marrow progenitor cells. However, enhanced megakaryopoiesis in BUBR1+/- mice was not correlated with a significant increase in platelets in peripheral blood, which was at least partly due to a defect in the formation of proplatelet-producing megakaryocytes. Together, BUBR1 is essential for early embryonic development and normal hematopoiesis. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: C. V. Rao, H. Y. Yamada, Y. Yao, and W. Dai Enhanced genomic instabilities caused by deregulated microtubule dynamics and chromosome segregation: a perspective from genetic studies in mice Carcinogenesis, September 1, 2009; 30(9): 1469 - 1474. [Abstract] [Full Text] [PDF] Q. Wen, C. Leung, Z. Huang, S. Small, A. L. Reddi, J. D. Licht, and J. D. Crispino Survivin is not required for the endomitotic cell cycle of megakaryocytes Blood, July 2, 2009; 114(1): 153 - 156. [Abstract] [Full Text] [PDF] M. Li, X. Fang, Z. Wei, J. P. York, and P. 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