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J. Biol. Chem., Vol. 281, Issue 14, 9227-9237, April 7, 2006

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The Interleukin-1 Gene Is Transcribed from a Poised Promoter Architecture in Monocytes^*

Michael D. Liang, Yue Zhang^¶, Daniel McDevit, Sylvia Marecki, and Barbara S. Nikolajczyk^¶1

From the Department of Pathology, Boston University School of Medicine, the Department of Medicine, Immunobiology Unit, Evans Memorial Department of Clinical Research, Boston Medical Center, and the ^¶Department of Microbiology, Boston University School of Medicine, Boston, Massachussetts 02118

Cytokine transcription is usually regulated by transcription factor binding and chromatin remodeling following an inducing signal. By contrast, these data showed the interleukin (IL)-1 promoter assembles into a "poised" structure, as evidenced by nuclease accessibility and loss of core histones immediately surrounding the transcription start site. Strikingly, these properties do not change upon transcriptional activation by lipopolysaccharide. Furthermore, association of two key transcriptional activators, PU.1 and C/EBP, is robust pre- and post-stimulation indicating the IL-1 promoter is packaged into a nontranscribed but poised promoter architecture in cells capable of rapidly inducing IL-1. Monocyte stimulation causes recruitment of a third factor, IRF-4, to the IL-1 enhancer. PU.1 phosphorylation at a CK2 kinase consensus element is required for this recruitment. We showed that CK2 phosphorylates PU.1, CK2 inhibitors abrogate IL-1 induction, and CK2 inducibly associates with the IL-1 enhancer. Taken together, these data indicate a novel two-step mechanism for IL-1 transcription: 1) formation of a poised chromatin architecture, and 2) phosphorylation of an enhancer-bound factor that recruits other activators. We propose that this poised structure may generally characterize rapidly activated genes.

Received for publication, September 30, 2005 , and in revised form, January 17, 2006.

^* This work was supported by an American Diabetes Association research grant and National Institutes of Health (NIH) Grant R01 AI54611 (to B. S. N.) and by NIH Grant T32 HL07501 and a Grunebaum Foundation fellowship (to M. D. L.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ To whom correspondence should be addressed: Dept. of Microbiology, Boston University School of Medicine, 715 Albany St. L516, Boston, MA 02118. Tel.: 617-638-7019; Fax: 617-638-4286; E-mail: bnikol{at}bumc.bu.edu.

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