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J Biol Chem, Vol. 275, Issue 2, 949-958, January 14, 2000
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.
Erythroid-specific Inhibition of the tal-1 Intragenic
Promoter Is Due to Binding of a Repressor to a Novel Silencer*
,
*
This work was supported in part by grants from the
"Association pour la Recherche sur le Cancer," the "Ligue
Nationale contre le Cancer," and the "Fondation contre la
Leucémie."The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Supported by a fellowship from the "Fondation pour la Recherche
Médicale."
§
Supported by a fellowship from the "Ligue Nationale contre le Cancer."
¶
To whom correspondence should be addressed. Tel.:
33-4-67-61-36-55; E-mail: mathieu@jones.igm.cnrs-mop.fr.
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