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Nucleic Acids Research 2005 33(13):3985-3993; doi:10.1093/nar/gki691
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Published online 19 July 2005

© The Author 2005. Published by Oxford University Press. All rights reserved
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions{at}oupjournals.org

Article

Interplay between positive and negative activities that influence the role of Bicoid in transcription

Dechen Fu and Jun Ma*

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 Avenue Cincinnati, OH 45229, USA

*To whom correspondence should be addressed. Tel: +1 513 636 7977; Fax: +1 513 636 4317; Email: jun.ma{at}cchmc.org

Received April 1, 2005. Revised May 20, 2005. Accepted June 16, 2005.

The Drosophila mophogenetic protein Bicoid (Bcd) can activate transcription in a concentration-dependent manner in embryos. It contains a self-inhibitory domain that can interact with the co-repressor Sin3A. In this report, we study a Bcd mutant, Bcd(A57–61), which has a strengthened self-inhibitory function and is unable to activate the hb-CAT reporter in Drosophila cells, to analyze the role of co-factors in regulating Bcd function. We show that increased concentrations of the co-activator dCBP in cells can switch this protein from its inactive state to an active state on the hb-CAT reporter. The C-terminal portion of Bcd(A57–61) is required to mediate such activity-rescuing function of dCBP. Although capable of binding to DNA in vitro, Bcd(A57–61) is unable to access the hb enhancer element in cells, suggesting that its DNA binding defect is only manifested in a cellular context. Increased concentrations of dCBP restore not only the ability of Bcd(A57–61) to access the hb enhancer element in cells but also the occupancy of the general transcription factors TBP and TFIIB at the reporter promoter. These and other results suggest that an activator can undergo switches between its active and inactive states through sensing the opposing actions of positive and negative co-factors.

Present address: Dechen Fu, Department of Molecular and Cellular Biology, University of California, Berkeley, CA 94720, USA


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