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J. Biol. Chem., Vol. 279, Issue 47, 48725-48733, November 19, 2004

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The Co-activator CREB-binding Protein Participates in Enhancer-dependent Activities of Bicoid^*

Dechen Fu, Ying Wen, and Jun Ma

From the Division of Developmental Biology, Cincinnati Children's Hospital Research Foundation, Graduate Program in Molecular and Developmental Biology, University of Cincinnati College of Medicine, Cincinnati, Ohio 45229

Bicoid (Bcd) is a transcriptional activator required for early embryonic patterning in Drosophila. Despite extensive studies, it currently remains unclear how Bcd activates transcription and what proteins participate in its activation process. In this report, we describe experiments to analyze the role of the Drosophila co-activator dCBP in Bcd-mediated activation. In Drosophila S2 cells, the Bcd activity is increased by the co-transfection of plasmids expressing dCBP and reduced by double-stranded RNA-mediated interference against dCBP. We further show that Bcd and dCBP can interact with each other and that Bcd-interacting domains of dCBP can cause dominant negative effects on Bcd activity in S2 cells. Our comparison of two Bcd-responsive enhancers, hunchback (hb) and knirps (kni), reveals a differential role of dCBP in facilitating Bcd activation. A dCBP mutant defective in its histone acetyltransferase activity exhibits a reduced, but not abolished, co-activator function for Bcd. Our chromatin immunoprecipitation experiments show that dCBP can increase not only the occupancy of Bcd itself at the enhancers but also the recruitment of general transcription factors to the promoter. Together, these experiments suggest that dCBP is an enhancer-dependent co-activator of Bcd, facilitating its activation through multiple mechanisms.

Received for publication, June 24, 2004 , and in revised form, August 16, 2004.

^* This study was supported by grants from the American Heart Association Grant 0255347N and National Science Foundation Grant 0323957 (to J. M.). 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.

To whom correspondence should be addressed: Division of Developmental Biology, Cincinnati Children's Hospital Research Foundation, Graduate Program in Molecular and Developmental Biology, University of Cincinnati College of Medicine, 3333 Burnet Ave., Cincinnati, OH 45229. Tel.: 513-636-7977; Fax: 513-636-4317; E-mail: jun.ma{at}cchmc.org.

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