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Blood, 1 May 2004, Vol. 103, No. 9, pp. 3342-3348. Prepublished online as a Blood First Edition Paper on January 15, 2004; DOI 10.1182/blood-2003-09-3202. This Article Full Text (PDF) All Versions of this Article: 2003-09-3202v1 103/9/3342    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 Curtis, D. J Articles by Begley, C G Search for Related Content PubMed PubMed Citation Articles by Curtis, D. J Articles by Begley, C G Related Collections Related Article in Blood Online Social Bookmarking                   What's this? Submitted September 22, 2003 Accepted January 1, 2004 SCL is required for normal function of short-term repopulating hematopoietic stem cells David J Curtis*, Mark A Hall, Leonie J Van Stekelenburg, Lorraine Robb, Stephen M Jane, and C G Begley Rotary Bone Marrow Research Laboratory, Royal Melbourne Hospital, Melbourne, Victoria, Australia Cancer & Haematology, The Walter and Eliza Hall Institute of Medical Research, Melbourne, Victoria, Australia Centre for Child Health Research, The Institute for Child Health Research, Perth, WA, Australia * Corresponding author; email: dcurtis{at}wehi.edu.au. SCL is essential for the development of hematopoietic stem cells in the embryo. Here, we used a conditional gene targeting approach to examine the function of SCL in adult hematopoietic stem cells (HSCs). Flow cytometry of bone marrow from SCL-deleted mice demonstrated a 4-fold increase in number of Linneg kit+ Sca-1+ cells. Despite this increase in the number of phenotypic HSCs, competitive repopulation assays demonstrated a severe multi-lineage defect in repopulation-capacity by SCL-deleted bone marrow cells. SCL-heterozygous cells also showed a mild repopulation defect, thus suggesting haplo-insufficiency of SCL. The transplantation defect of SCL-deleted cells was observed within 4 weeks of transplant, indicating a defect in a multi-potent progenitor or short-term repopulating HSC. Although the defect persisted in secondary transplants, it remained relatively stable, suggesting that SCL was not required for self-renewal of the HSC. Generation of SCL-deleted cells within SCL-wild type mice rescued the early repopulating defect. Together, our results suggest that SCL is required for the normal function of short-term repopulating HSCs. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: The "stem cell leukemia" gene: what's in a name? 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