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Originally published In Press as doi:10.1074/jbc.M200924200 on May 21, 2002

J. Biol. Chem., Vol. 277, Issue 30, 27144-27153, July 26, 2002
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GATA Factors Are Essential for Transcription of the Survival Gene E4bp4 and the Viability Response of Interleukin-3 in Ba/F3 Hematopoietic Cells*

Yung-Luen YuDagger §, Yun-Jung Chiang§, and Jeffrey J. Y. Yen§

From the Dagger  Graduate Institute of Life Sciences, National Defense Medical Center and the § Institute of Biomedical Sciences, Academia Sinica, Taipei, 115 Taiwan

E4bp4, a member of the basic region/leucine zipper transcription factor superfamily, is up-regulated by the interleukin-3 (IL-3) signaling pathway and plays an important role in the anti-apoptotic response of IL-3. In this study, we demonstrated that E4bp4 is regulated by IL-3 mainly at the transcriptional level. Promoter analysis revealed that a GATA motif downstream of a major transcription initiation site is essential for E4bp4 expression in the IL-3-dependent Ba/F3 cell line. Gel shift assays demonstrated that both GATA-1 and GATA-2 proteins bind to the E4bp4 GATA site in vitro, and the chromatin immunoprecipitation assay further confirmed the in vivo binding of GATA-1 to the E4bp4 promoter. Overexpression of GATA-1 alone transactivates the E4bp4 reporter, whereas transactivation of the E4bp4 reporter by GATA-2 is dependent on the stimulation of IL-3. Last, we demonstrated that alteration of GATA-1 binding to the GATA site by stably overexpressing GATA-1 or a GATA-1 mutant containing only the DNA-binding domain not only modulates the expression of the E4bp4 gene but also influences apoptosis induced by IL-3 removal. Taken together, our results suggest that the GATA factors play an important role in transducing the survival signal of IL-3, and one of their cellular targets is E4bp4.

* This work was supported in part by an intramural fund from Academia Sinica, Taiwan (to J. J.-Y. Y.) and Grants NSC86-2314-B-001-026 and NSC88-2314-B-001-018 from the National Science Council of Taiwan (to J. J.-Y. Y.).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: Inst. of Biomedical Sciences, Academia Sinica. No. 128, Sec. 2, Yen-Jiou-Yuan Rd., Taipei, 115 Taiwan. Tel.: 886-2-2652-3077; Fax: 886-2-2782-9142; E-mail: bmjyen@ibms.sinica.edu.tw.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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