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Blood, 15 November 2007, Vol. 110, No. 10, pp. 3601-3609.
Prepublished online as a Blood First Edition Paper on August 3, 2007; DOI 10.1182/blood-2007-04-086827.
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Submitted April 24, 2007
Accepted July 26, 2007
Mouse lycat controls the development of hematopoietic and endothelial lineages during in vitro ES cell differentiation
Chengyan Wang, Patrick W Faloon, Zhijia Tan, Yaxin Lv, Pengbo Zhang, Yu Ge, Hongkui Deng, and Jing-Wei Xiong*
Key Laboratory of Cell Proliferation, & Differentiation of the Ministry of Education, College of Life Sciences, Peking University, Beijing, China
The Cardiovascular Research Center, Massachusetts General Hospital & Harvard Medical School, Charlestown, MA, United States
Nephrology Division, Massachusetts General Hospital & Harvard Medical School, Charlestown, MA, United States
* Corresponding author; email: xiong{at}cvrc.mgh.harvard.edu.
The blast-colony-forming cell (BL-CFC) was identified as an equivalent to the hemangioblast during in vitro ES cell differentiation. However, it remains largely unknown what are the molecular mechanisms underlying the generation of the BL-CFC. Here we report the isolation of mouse lysocardiolipin acyltransferase (Lycat) based on homology to zebrafish lycat, a candidate gene for the cloche locus. Mouse Lycat is expressed in hematopoietic organs and is enriched in the Lin-C-Kit+Sca-1+ hematopoietic stem cells in bone marrow and in the Flk1+/hCD4+(Scl+) hemangioblast population in embryoid bodies. The forced Lycat transgene leads to increased mRNA expression of hematopoietic and endothelial genes as well as increased blast colonies and their progenies, endothelial and hematopoietic lineages. The Lycat siRNA transgene leads to a decrease expression of hematopoietic and endothelial genes. An unbiased genome-wide microarray analysis further substantiates that the forced Lycat transgene specifically up-regulates a set of genes related to hemangioblasts, hematopoietic and endothelial lineages. Therefore, mouse Lycat plays an important role in the early specification of hematopoietic and endothelial cells, probably acting at the level of the hemangioblast.
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