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Repression of Id2 expression by Gfi-1 is required for B-cell and myeloid development

  1. Author:
    Li, H. J.
    Ji, M.
    Klarmann, K. D.
    Keller, J. R.

  2. Author Address

    [Li, Huajie; Ji, Ming; Klarmann, Kimberly D.; Keller, Jonathan R.] NCI, Basic Res Program, SAIC Frederick Inc, Ctr Canc Res, Frederick, MD 21702 USA.;Keller, JR, NCI, Basic Res Program, SAIC Frederick Inc, Ctr Canc Res, Bldg 560,Rm 12-03, Frederick, MD 21702 USA.;kellerjo@mail.nih.gov
    1. Year: 2010
    2. Date: Aug 19
    3. Epub Date: 5/11/2010
  2. Journal: Blood
    1. 116
    2. 7
    3. Pages: 1060-1069
  4. Type of Article: Article
  5. ISSN: 0006-4971
  1. Abstract:

    The development of mature blood cells from hematopoietic stem cells requires coordinated activities of transcriptional networks. Transcriptional repressor growth factor independence 1 (Gfi-1) is required for the development of B cells, T cells, neutrophils, and for the maintenance of hematopoietic stem cell function. However, the mechanisms by which Gfi-1 regulates hematopoiesis and how Gfi-1 integrates into transcriptional networks remain unclear. Here, we provide evidence that Id2 is a transcriptional target of Gfi-1, and repression of Id2 by Gfi-1 is required for B-cell and myeloid development. Gfi-1 binds to 3 conserved regions in the Id2 promoter and represses Id2 promoter activity in transient reporter assays. Increased Id2 expression was observed in multipotent progenitors, myeloid progenitors, T-cell progenitors, and B-cell progenitors in Gfi-1(-/-) mice. Knockdown of Id2 expression or heterozygosity at the Id2 locus partially rescues the B-cell and myeloid development but not the T-cell development in Gfi-1(-/-) mice. These studies demonstrate a role of Id2 in mediating Gfi-1 functions in B-cell and myeloid development and provide a direct link between Gfi-1 and the B-cell transcriptional network by its ability to repress Id2 expression. (Blood. 2010;116(7):1060-1069)

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External Sources

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  2. DOI: 10.1182/blood-2009-11-255075
  3. PMID: 20453161
  4. PMCID: PMC2938128
  5. View record in Web of Science®
  6. WOS: 000281117500010

Library Notes

  1. Fiscal Year: FY2009-2010
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