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Journal Article

Bicoid: Morphogen function revisited


Löhr,  U.
Max Planck Society;


Chung,  H. R.
Computational Epigenetics (Ho-Ryun Chung), Independent Junior Research Groups (OWL), Max Planck Institute for Molecular Genetics, Max Planck Society;

Beller,  M.
Max Planck Society;

Jäckle,  H.
Max Planck Society;

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Löhr, U., Chung, H. R., Beller, M., & Jäckle, H. (2010). Bicoid: Morphogen function revisited. Fly (Austin), 4(3), 236-240. Retrieved from http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=20404518.

Cite as: http://hdl.handle.net/11858/00-001M-0000-0010-7AAF-7
Bicoid (Bcd) functions as a morphogen during Drosophila development. Accordingly, bcd mRNA is maternally localized to the anterior pole of the embryo, and Bcd forms an anterior/posterior gradient, which functions in a concentration dependent fashion. Thus, nuclei receiving identical amounts of Bcd should express the same target genes. However, we found that ectopic, uniform expression of Bcd causes anterior gene expression in the posterior with mirror image polarity, indicating that one or several additional factors must provide positional information. Recently, we have shown that one of these factors is Capicua (Cic), a ubiquitous maternal repressor that is downregulated at the embryonic termini by maternal Torso, a key component of the maternal terminal system. Cic acts on Bcd dependent enhancer elements by repression and thereby controls the posterior limit of Bcd target gene expression. Based on these new findings, we propose that spatial control of gene expression in the anterior region of the embryo is not solely the result of Bcd morphogen action. Rather, it relies on a "morphogenic network" that integrates the terminal system and Bcd activities, providing both polarity and spatial information to the prospective head region of the developing embryo.