Mutations in the Murine Fitness 1 Gene Result in Defective Hematopoiesis
Mark D. Potter,
Sarah G. Shinpock,
Raymond A. Popp,
Diana M. Popp,
Virginia Godfrey,
Donald A. Carpenter,
Alan Bernstein,
Dabney K. Johnson, and
Eugene M. Rinchik
From the University of Tennessee-Oak Ridge Graduate School of Biomedical Sciences, and the Biology Division of the Oak Ridge National Laboratory, Oak Ridge, TN; Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Canada; the Department of Medical Genetics, University of Toronto, Toronto, Canada; and Sarah Lawrence College, Bronxville, NY.
Identification and characterization of mutations that disrupt normal hematopoiesis are essential for understanding the genetic pathways that control the development and regulation of the mammalian hematopoietic system. Previously, the fitness 1 gene was identified by five, independent mutations in N-ethyl-N-nitrosourea (ENU) saturation mutagenesis experiments within the albino (c) region of mouse chromosome 7 (MMU7). We report here that fit1 mutants are anemic, display numerous peripheral blood defects, and are deficient in early hematopoietic progenitor cell populations. The number of both erythroid and myeloid progenitors, as well as B cells, are reduced. These results implicate fit1 involvement in normal hematopoiesis and suggest that further characterization of the fit1 gene, and the five presumed point mutations of the gene, will lead to an improved understanding of normal hematopoiesis in the mouse.
Blood, Vol. 90 No. 5 (September 1), 1997:
pp. 1850-1857
© 1997 by The American Society of Hematology.
