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Molecular and Cellular Biology, September 1998, p. 5414-5424, Vol. 18, No. 9
0270-7306/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Stress-Induced Fas Ligand Expression in T Cells Is Mediated through a MEK Kinase 1-Regulated Response Element in the Fas Ligand Promoter

Mary Faris,1 Kevin M. Latinis,2 Stephan J. Kempiak,1 Gary A. Koretzky,2 and Andre Nel1,*

Division of Clinical Immunology and Allergy, Department of Medicine, UCLA School of Medicine, Los Angeles, California 90095,1 and Department of Internal Medicine and Interdisciplinary Graduate Program in Immunology, University of Iowa, Iowa City, Iowa 522422

Received 20 February 1998/Returned for modification 16 April 1998/Accepted 22 June 1998

T lymphocytes undergo apoptosis in response to a variety of stimuli, including exposure to UV radiation and gamma -irradiation. While the mechanism by which stress stimuli induce apoptosis is not well understood, we have previously shown that the induction of Fas ligand (FasL) gene expression by environmental stress stimuli is dependent on c-Jun N-terminal kinase (JNK) activation. Using inducible dominant-active (DA) JNK kinase kinase (MEKK1) expression in Jurkat cells, we map a specific MEKK1-regulated response element to positions -338 to -316 of the Fas ligand (FasL) promoter. Mutation of that response element abrogated MEKK1-mediated FasL promoter activation and interfered in stress-induced activation of that promoter. Using electrophoretic mobility shift assays, we demonstrate that activator protein 1 (AP-1) binding proteins, namely, activating transcription factor 2 (ATF2) and c-Jun, bind to the MEKK1 response element. Transient transfection of interfering c-Jun and ATF2 mutants, which lack the consensus JNK phosphorylation sites, abrogated the transcriptional activation of the FasL promoter, demonstrating the involvement of these transcription factors in the regulation of the FasL promoter. Taken together, our data indicate that MEKK1 and transcription factors regulated by the JNK pathway play a role in committing lymphocytes to undergo apoptosis by inducing FasL expression via a novel response element in the promoter of that gene.

* Corresponding author. Mailing address: UCLA School of Medicine, Department of Medicine, 52-175 CHS, 10833 Le Conte Ave., Los Angeles, CA 90095. Phone: (310) 825-6620. Fax: (310) 206-8107. E-mail: anel{at}med1.medsch.ucla.edu.

Molecular and Cellular Biology, September 1998, p. 5414-5424, Vol. 18, No. 9
0270-7306/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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