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J. Biol. Chem., Vol. 277, Issue 21, 18313-18321, May 24, 2002
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From the Using a transgenic approach, we studied the role
of GATA-3 in T cells. As previously shown, enforced GATA-3 expression
in transgenic mice inhibits Th1 differentiation of CD4 T cells, but unexpectedly, both type 1 (interferon
Interleukin-13 Gene Expression Is Regulated by GATA-3 in T
Cells
ROLE OF A CRITICAL ASSOCIATION OF A GATA AND TWO GATG
MOTIFS*
§,,, and
Institut Cochen (INSERM, CNRS,
Université Paris V), Département d'Hematologie, Maternite
Port-Royal, 123 Bd de Port-Royal, 75014 Paris, France and
¶ Laboratory of Molecular Biology, NIDDK, National Institutes of
Health, Bethesda, Maryland 20892
) and type 2 (interleukin (IL)-4 and IL-13) cytokine genes were activated in the transgenic CD8 T
cells. Because IL-13 gene expression was highly enhanced in
vivo by GATA-3 expression, we studied the human and the mouse IL-13 gene promoters and found an evolutionary-conserved association of
a consensus GATA binding site and two GATG motifs. We showed that
efficient GATA-3 binding to this regulatory sequence required these
three motifs and that the affinity of the GATA zinc fingers for this
association was five times higher than for the consensus GATA binding
site alone. Transfections in a T cell line or transactivation by GATA-3
showed that the combination of the three sites was required for full
transcriptional activity of the IL-13 gene promoter. Finally we showed
that this association of binding sites causes a very high sensitivity
of the IL-13 gene promoter to small variations in the level of GATA-3
protein. Altogether, these results indicate an important role of GATA-3
in CD8 cytokine gene expression and demonstrate that a critical network
of GATA binding sites highly modulates GATA-3 activity.
*
This work was supported in part by grants from the INSERM
and the Ligue Nationale Contre Le Cancer (Equipe Labellisée).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.
To whom correspondence should be addressed. Tel.:
33-153104384; Fax: 033-143251167; E-mail:
maxaudit@cochin.inserm.fr.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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