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Blood, 15 March 2004, Vol. 103, No. 6, pp. 2343-2350. Prepublished online as a Blood First Edition Paper on November 20, 2003; DOI 10.1182/blood-2003-06-1852. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-06-1852v1 103/6/2343    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map 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 Turcotte, K. Articles by Gros, P. Search for Related Content PubMed PubMed Citation Articles by Turcotte, K. Articles by Gros, P. Related Collections Hematopoiesis and Stem Cells Neoplasia Genomics Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Genetic control of myeloproliferation in BXH-2 mice Karine Turcotte, Susan Gauthier, Loukia-Maria Mitsos, Chaim Shustik, Neal G. Copeland, Nancy A. Jenkins, Jean-Christophe Fournet, Paul Jolicoeur, and Philippe Gros From the Department of Biochemistry, McGill University, Montreal, QC, Canada; the Department of Hematology, Royal Victoria Hospital, Montreal, QC, Canada; the Mouse Cancer Genetics Program, National Cancer Institute, Frederick, MD; the Department of Pathology, Hôpital Ste-Justine, Montreal, QC, Canada; the Department of Molecular Biology, the Clinical Research Institute of Montreal, Montreal, QC, Canada; the Department of Experimental Medicine, McGill University, Montreal, QC, Canada; and the Department of Microbiology and Immunology, Université de Montréal, Montreal, QC, Canada. While studying the unique Nramp1 (Slc11a1)–independent susceptibility to Mycobacterium bovis (BCG) infection of BXH-2 mice, we noted that these mice develop important splenomegaly and enlargement of lymph nodes. Segregation analyses in several F2 crosses showed that splenomegaly segregates as a single recessive trait caused by a novel mutation in BXH-2, independent of the infection. Histologic and fluorescence-activated cell sorter (FACS) analyses indicated that splenomegaly is associated with a large increase in Mac1+/GR1+ (macrophage antigen-1+/granulocyte differentiation antigen 1+) granulocyte precursors in spleen, lymph nodes, and bone marrow, resembling a myeloproliferative syndrome. This is concomitant to extramedullary erythropoiesis in the spleen, as measured by proportion of Ter119+ erythroid cells. The locus controlling this myeloproliferative syndrome and splenomegaly was designated Myls and maps to an 18 centimorgan (cM) region of chromosome 8, which also contains an integrated copy of an N-ecotropic murine leukemia virus (MuLV) provirus (Emv2). The relationship between Myls, expansion of Mac1+/GR1+ cells, and Emv2 was investigated. Homozygosity at Myls is necessary but not sufficient for B-ecotropic virus replication in splenocytes, the extent of which appears to be under separate genetic control. Our results suggest a model in which Myls-dependent myeloproliferation in BXH-2 acts as a predisposing factor for the subsequent development of virally induced myeloid leukemia characteristic of this strain. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: A. Fortier, K. Doiron, M. Saleh, S. Grinstein, and P. Gros Restriction of Legionella pneumophila Replication in Macrophages Requires Concerted Action of the Transcriptional Regulators Irf1 and Irf8 and Nod-Like Receptors Naip5 and Nlrc4 Infect. Immun., November 1, 2009; 77(11): 4794 - 4805. [Abstract] [Full Text] [PDF] P. Tailor, T. Tamura, H. C. Morse III, and K. Ozato The BXH2 mutation in IRF8 differentially impairs dendritic cell subset development in the mouse Blood, February 15, 2008; 111(4): 1942 - 1945. [Abstract] [Full Text] [PDF] K. Turcotte, S. Gauthier, D. Malo, M. Tam, M. M. Stevenson, and P. Gros Icsbp1/IRF-8 Is Required for Innate and Adaptive Immune Responses against Intracellular Pathogens J. Immunol., August 15, 2007; 179(4): 2467 - 2476. [Abstract] [Full Text] [PDF] K. Turcotte, S. Gauthier, A. Tuite, A. Mullick, D. Malo, and P. Gros A mutation in the Icsbp1 gene causes susceptibility to infection and a chronic myeloid leukemia-like syndrome in BXH-2 mice J. Exp. Med., March 21, 2005; 201(6): 881 - 890. [Abstract] [Full Text] [PDF]

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