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This version published online on September 6, 2007
Molecular Endocrinology, doi:10.1210/me.2007-0211
A more recent version of this article appeared on December 1, 2007
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*2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN

Submitted on April 24, 2007
Accepted on August 28, 2007

RELB, A NEW PARTNER OF ARYL HYDROCARBON RECEPTOR-MEDIATED TRANSCRIPTION

Christoph F. A. Vogel*, Eric Sciullo, Wen Li, Pat Wong, Gwendal Lazennec, and Fumio Matsumura

Department of Environmental Toxicology, University of California, Davis, One Shields Avenue, Davis, CA 95616; INSERM U540 ‘Molecular and Cellular Endocrinology of Cancers’, 60, rue de Navacelles, 34090 Montpellier, France

* To whom correspondence should be addressed. E-mail: cfvogel{at}ucdavis.edu.

The NF-{kappa}B transcription factor family has a crucial role in rapid responses to stress and pathogens. We show that the NF-{kappa}B subunit RelB is functionally associated with the aryl hydrocarbon receptor (AhR) and mediates transcription of chemokines such as Interleukin-8 (IL-8) via activation of AhR and protein kinase A (PKA). RelB physically interacts with AhR and binds to an unrecognized RelB/AhR responsive element (RelBAhRE) of the IL-8 promoter linking two signaling pathways to activate gene transcription. We found a time-dependent recruitment of AhR to the RelBAhRE site of IL-8 mediated by the AhR ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, dioxin) and via activation of PKA. Furthermore, NF-{kappa}B-binding sites that are preferentially recognized by RelB/p52 are a target for RelB/AhR complexes without addition of any stimuli implicating the endogenous function of the AhR. RelB/AhR complexes are also found to bind on Xenobiotic Responsive Elements (XRE), and RelB drastically increases the TCDD-induced XRE reporter activity. The interaction of RelB with AhR signaling, and AhR with NF-{kappa}B RelB signaling pathways represent a new mechanism of cross talk between the two transcription factors.
Key words: AhR • chemokines • IL-8 • NF-{kappa}B • RelB • TCDD




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