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Development, Vol 128, Issue 10 1869-1879, Copyright © 2001 by Company of Biologists
JOURNAL ARTICLES |
RD Flores-Saaib, S Jia and AJ Courey
Department of Chemistry and Biochemistry, University of California, Los Angeles, CA 90095-1569, USA. courey@chem.ucla.edu
In the Drosophila embryo, Dorsal, a maternally expressed Rel family transcription factor, regulates dorsoventral pattern formation by activating and repressing zygotically active fate-determining genes. Dorsal is distributed in a ventral-to-dorsal nuclear concentration gradient in the embryo, the formation of which depends upon the spatially regulated inhibition of Dorsal nuclear uptake by Cactus. Using maternally expressed Gal4/Dorsal fusion proteins, we have explored the mechanism of activation and repression by Dorsal. We find that a fusion protein containing the Gal4 DNA-binding domain fused to full-length Dorsal is distributed in a nuclear concentration gradient that is similar to that of endogenous Dorsal, despite the presence of a constitutively active nuclear localization signal in the Gal4 domain. Whether this fusion protein activates or represses reporter genes depends upon the context of the Gal4-binding sites in the reporter. A Gal4/Dorsal fusion protein lacking the conserved Rel homology domain of Dorsal, but containing the non-conserved C-terminal domain also mediates both activation and repression, depending upon Gal4-binding site context. A region close to the C-terminal end of the C-terminal domain has homology to a repression motif in Engrailed - the eh1 motif. Deletion analysis indicates that this region mediates transcriptional repression and binding to Groucho, a co-repressor known to be required for Dorsal-mediated repression. As has previously been shown for repression by Dorsal, we find that activation by Dorsal, in particular by the C-terminal domain, is modulated by the maternal terminal pattern-forming system.
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S. Jia, R. D. Flores-Saaib, and A. J. Courey The Dorsal Rel Homology Domain Plays an Active Role in Transcriptional Regulation Mol. Cell. Biol., July 15, 2002; 22(14): 5089 - 5099. [Abstract] [Full Text] [PDF]
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