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Originally published In Press as doi:10.1074/jbc.M107068200 on January 10, 2002

J. Biol. Chem., Vol. 277, Issue 12, 10704-10711, March 22, 2002
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Regulation of the Murine Nfatc1 Gene by NFATc2*

Bin ZhouDagger §, Randy Q. Cron§, Bingruo WuDagger , Anna Genin, Zhili Wang||, Steve LiuDagger , Paul RobsonDagger , and H. Scott BaldwinDagger **

From the Divisions of Dagger  Cardiology and  Rheumatology, Department of Pediatrics, and the || Nucleic Acid and Protein Core, Joseph Stokes, Jr. Research Institute, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104-4318

NFAT proteins play a key role in the inducible expression of cytokine genes in T lymphocytes. NFATc1 and NFATc2 are the predominant NFAT family members in the peripheral immune system. NFATc2 is found abundantly in the cytoplasm of resting T cells, whereas Nfatc1 expression is induced during T cell activation. To investigate Nfatc1 regulation, we characterized the structure of the murine Nfatc1 gene and its 5'-flanking region. A 290-bp sequence proximal to the transcription start site is highly conserved between mouse and human and possesses both basal and inducible promoter activities. Multiple binding sites for transcription factors were identified within this region, including a consensus NFAT-binding site. This promoter segment was cyclosporin A-sensitive, and mutation of the NFAT site abrogated inducible promoter activity and inhibited formation of an inducible DNA·protein complex containing NFATc2 in primary T cells. Overexpression of NFATc2 increased inducible Nfatc1 promoter activity, whereas this inducibility was attenuated in NFATc2-/- splenocytes. This study suggests that pre-existing NFATc2 contributes to the subsequent induction of Nfatc1 during T cell activation.

* This work was supported by Grant P50HL62177 from the National Institutes of Health (to H. S. B.) and the Elizabeth Glaser Pediatric AIDS Foundation Grant PF-77638 (to R. Q. C.) and by postdoctoral fellowships from the American Heart Association (to B. Z. and P. R.).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.

§ Both authors contributed equally to this work.

** To whom correspondence should be addressed: Children's Hospital of Philadelphia, 3615 Civic Center Blvd., ARC 702, Philadelphia, PA 19104-4318. Tel.: 215-590-2938; Fax: 215-590-5454; E-mail: sbaldwin@mail.med.upenn.edu.

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