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The basic helix-loop-helix transcription factor TAL1/SCL inhibits the expression of the p16INK4A and pTalpha genes

Anders Hansson1, Christina Manetopoulos, Jan Ingvar Jönsson

  • 1Department of Laboratory Medicine, Division of Molecular Medicine, Lund University, University Hospital MAS, SE-205 02, Malmö, Sweden.

Biochemical and Biophysical Research Communications
|December 4, 2003
PubMed

The Tal1 gene (also called Scl or TCL5) encodes a basic helix-loop-helix transcription factor required for hematopoiesis and vasculogenesis. Additionally, aberrant transcriptional activation of the Tal1 gene is a frequent event in human T cell acute lymphoblastic leukemia (T-ALL). T cell specific expression of TAL1 in mice induces aggressive T cell malignancies, demonstrating the oncogenic potential of TAL1. Yet, the underlying mechanisms of TAL1 induced tumorigenesis are poorly understood. By inhibiting E protein mediated transcription of the pTalpha gene, TAL1 can interfere with the T cell differentiation program. In addition, several studies suggest that TAL1 expression might also enhance proliferation rate. We report here that TAL1 can bind the E boxes in both the p16 and the pTalpha promoters, and functionally suppress the activity of both promoters. These results indicate that TAL1 can affect both T cell proliferation and differentiation. Moreover, we show that overexpression of TAL1 in hematopoietic progenitor cells promotes cell cycle division.

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