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J Biol Chem, Vol. 275, Issue 2, 949-958, January 14, 2000

Erythroid-specific Inhibition of the tal-1 Intragenic Promoter Is Due to Binding of a Repressor to a Novel Silencer^*

Christine Courtes, Nathalie Lecointe, Laurent Le Cam^§, Florence Baudoin, Claude Sardet, and Danièle Mathieu-Mahul^¶

From the Institut de Génétique Moléculaire, UMR 5535, IFR 24, 1919 Route de Mende, F 34293, Montpellier, France

The basic helix-loop-helix tal-1 gene plays a key role in hematopoiesis, and its expression is tightly controlled through alternative promoters and complex interactions of cis-acting regulatory elements. tal-1 is not expressed in normal T cells, but its transcription is constitutive in a large proportion of human T cell leukemias. We have previously described a downstream initiation of tal-1 transcription specifically associated with a subset of T cell leukemias that leads to the production of NH₂-truncated TAL-1 proteins. In this study, we characterize the human promoter (promoter IV), embedded within a GC-rich region in exon IV, responsible for this transcriptional activity. The restriction of promoter IV usage is assured by a novel silencer element in the 3'-unstranslated region of the human gene that represses its activity in erythroid but not in T cells. The silencer activity is mediated through binding of a tissue-specific nuclear factor to a novel protein recognition motif (designated tal-RE) in the silencer. Mutation of a single residue within the tal-RE abolishes both specific protein binding and silencing activity. Altogether, our results demonstrate that the tal-1 promoter IV is actively repressed in cells of the erythro-megakaryocytic lineage and that this repression is released in leukemic T cells, resulting in the expression of the tal-1 truncated transcript.

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