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Blood, 15 November 2007, Vol. 110, No. 10, pp. 3573-3581. Prepublished online as a Blood First Edition Paper on July 20, 2007; DOI 10.1182/blood-2006-10-053124. This Article Full Text (PDF) All Versions of this Article: blood-2006-10-053124v1 110/10/3573    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 Salmon, J. M Articles by Curtis, D. J Search for Related Content PubMed PubMed Citation Articles by Salmon, J. M Articles by Curtis, D. J Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted October 19, 2006 Accepted June 27, 2007 Aberrant mast cell differentiation in mice lacking the stem cell leukemia gene Jessica M Salmon, Nicholas J Slater, Mark A Hall, Matthew P McCormack, Stephen L Nutt, Stephen M Jane, and David J Curtis* Rotary Bone Marrow Research Laboratories, Royal Melbourne Hospital, Melbourne, Australia Immunology Division, The Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia * Corresponding author; email: dcurtis{at}wehi.edu.au. The stem cell leukemia (SCL) gene encodes a basic helix-loop-helix transcription factor expressed in erythroid, megakaryocyte and mast cell lineages. SCL is essential for growth of megakaryocyte and erythroid progenitors. We have used a conditional knockout of SCL (SCL-/) to examine its function in mast cells, critical effectors of the immune system. SCL-/ mice had markedly increased numbers of mast cell progenitors (MCP) within the peritoneal fluid, bone marrow and spleen. Fractionation of bone marrow myeloid progenitors demonstrated that these MCP were present in the megakaryocyte-erythroid-restricted cell fraction. In contrast, uni-lineage MCP from control mice were present in the cell fraction with granulocyte-macrophage potential. The aberrant mast cell differentiation of SCL-/ megakaryocyte-erythroid progenitors was associated with increased expression of GATA-2. Despite increased numbers of MCP in SCL-/ mice, numbers of mature, tissue mast cells were not increased unless SCL-/ mice were treated with IL-3 and stem cell factor. In part, this may be due to a requirement for SCL in normal mast cell maturation: SCL-/ mast cells had reduced expression of the high-affinity IgE receptor and mast cell proteases, MCP-5 and MCP-6. Together, these studies suggest that loss of SCL leads to aberrant mast cell differentiation of megakaryocyte-erythroid progenitors. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: M. T. Kassouf, H. Chagraoui, P. Vyas, and C. Porcher Differential use of SCL/TAL-1 DNA-binding domain in developmental hematopoiesis Blood, August 15, 2008; 112(4): 1056 - 1067. [Abstract] [Full Text] [PDF] D. Metcalf, I. Majewski, S. Mifsud, L. Di Rago, and W. S. Alexander Clonogenic mast cell progenitors and their excess numbers in chimeric BALB/c mice with inactivated GATA-1 PNAS, November 20, 2007; 104(47): 18642 - 18647. [Abstract] [Full Text] [PDF]

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