Published online 6 May 2004
Nucleic Acids Research, 2004, Vol. 32, No. 8 2508-2519
© 2004 Oxford University Press
Targeted transcriptional repression of Gfi1 by GFI1 and GFI1B in lymphoid cells
1 Institute for Cellular Therapeutics, 2 Department of Biochemistry and Molecular Biology and 8 Department of Surgery, University of Louisville, KY, USA, 3 Genetic Pathology Evaluation Centre, University of British Columbia, Vancouver, BC, Canada, 4 Department of Medicine, University of Washington School of Medicine, Seattle, WA, USA, 5 Molecular Oncology, Fox Chase Cancer Center, Philadelphia, PA, USA, 6 Molecular Oncology Research Institute, Tufts-New England Medical Center, Boston, MA, USA and 7 Department of Pathology, Vancouver General Hospital, BC, Canada
*To whom correspondence should be addressed. Tel: +1 502 852 2080; Fax: +1 502 852 2079; Email: lee.grimes{at}louisville.edu
Received February 10, 2004; Revised and Accepted April 6, 2004
Growth factor independence-1 (GFI1) and GFI1B are closely related, yet differentially expressed transcriptional repressors with nearly identical DNA binding domains. GFI1 is upregulated in the earliest thymocyte precursors, while GFI1B expression is restricted to T lymphopoiesis stages coincident with activation. Transgenic expression of GFI1 potentiates T-cell activation, while forced GFI1B expression decreases activation. Both mice and humans with mutant Gfi1 display lymphoid abnormalities. Here we describe autoregulation of Gfi1 in primary mouse thymocytes and a human T-cell line. GFI1 binding to cis-element sequences conserved between rat, mouse and human Gfi1 mediates direct and potent transcriptional repression. In addition, dramatic regulation of Gfi1 can also be mediated by GFI1B. These data provide the first example of a gene directly targeted by GFI1 and GFI1B. Moreover, they support a role for auto- and trans-regulation of Gfi1 by GFI1 and GFI1B in maintaining the normal expression patterns of Gfi1, and suggest that GFI1B may indirectly affect T-cell activation through repression of Gfi1.
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