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Bcl11a is essential for normal lymphoid development

  1. Author:
    Liu, P. T.
    Keller, J. R.
    Ortiz, M.
    Tessarollo, L.
    Rachel, R. A.
    Nakamura, T.
    Jenkins, N. A.
    Copeland, N. G.

  2. Author Address

    NCI, Mouse Canc Genet Program, Frederick, MD 21702 USA NCI, Mouse Canc Genet Program, Frederick, MD 21702 USA NCI, SAIC Frederick Inc, Basic Res Program, Frederick, MD 21702 USA Japanese Fdn Canc Res, Toshima Ku, Tokyo 1708455, Japan Copeland NG NCI, Mouse Canc Genet Program, Frederick, MD 21702 USA
    1. Year: 2003
  2. Journal: Nature Immunology
    1. 4
    2. 6
    3. Pages: 525-532
  4. Type of Article: Article
  1. Abstract:

    Bcl11a (also called Evi9) functions as a myeloid or B cell proto-oncogene in mice and humans, respectively. Here we show that Bcl11a is essential for postnatal development and normal lymphopoiesis. Bcl11a mutant embryos lack B cells and have alterations in several types of T cells. Phenotypic and expression studies show that Bcl11a functions upstream of the transcription factors Ebf1 and Pax5 in the B cell pathway. Transplantation studies show that these defects in Bcl11a mutant mice are intrinsic to fetal liver precursor cells. Mice transplanted with Bcl11a-deficient cells died from T cell leukemia derived from the host. Thus, Bcl11a may also function as a non-autonomous T cell tumor suppressor gene.

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