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Molecular and Cellular Biology, May 2000, p. 3407-3416, Vol. 20, No. 10
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Bcl-3 Expression Promotes Cell Survival following Interleukin-4 Deprivation and Is Controlled by AP1 and AP1-Like Transcription Factors

Angelita Rebollo,1,* Laure Dumoutier,2 Jean-Christophe Renauld,2 Angel Zaballos,1 Verónica Ayllón,1 and Carlos Martínez-A.1

Centro Nacional de Biotecnología, Department of Immunology and Oncology, UAM, E-28049 Madrid, Spain,1 and Ludwig Institute for Cancer Research, UCL 74.59, B-1200, Brussels, Belgium2

Received 18 October 1999/Returned for modification 9 December 1999/Accepted 14 February 2000

We have analyzed the interleukin-4 (IL-4)-triggered mechanisms implicated in cell survival and show here that IL-4 deprivation induces apoptotic cell death but does not modulate Bcl-2 or Bcl-x expression. Since Bcl-x expression is insufficient to ensure cell survival in the absence of IL-4, we speculate that additional molecules replace the antiapoptotic role of Bcl-2 and Bcl-x in an alternative IL-4-triggered pathway. Cell death is associated with Bcl-3 downregulation and Bcl-3 expression blocks IL-4 deprivation-induced apoptosis, suggesting that Bcl-3 acts as a survival factor in the absence of growth factor. To characterize the IL-4-induced regulation of murine Bcl-3 expression, we cloned the promoter of this gene. Sequencing of the promoter showed no TATA box element but did reveal binding sites for AP1, AP1-like, and SP1 transcription factors. Retardation gels showed that IL-4 specifically induces AP1 and AP1-like binding activity and that mutation of these binding sites abolishes the IL-4-induced Bcl-3 promoter activity, suggesting that these transcription factors are important in Bcl-3 promoter transactivation. IL-4 deprivation induces downregulation of Jun expression and upregulation of Fos expression, both of which are proteins involved in the formation of AP1 and AP1-like transcription factors. Overexpression of Jun family proteins transactivates the promoter and restores Bcl-3 expression in the absence of IL-4 stimulation. Taken together, these data describe a new biological role for Bcl-3 and define the regulatory pathway implicated in Bcl-3 expression.

* Corresponding author. Mailing address: Centro Nacional de Biotecnología, Department of Immunology and Oncology, Campus de Cantoblanco, UAM 28049 Madrid, Spain. Phone: (34) 91/585-4655. Fax: (34) 91/585-4506. E-mail: arebollo{at}cnb.uam.es.

Molecular and Cellular Biology, May 2000, p. 3407-3416, Vol. 20, No. 10
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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