@article {843376,
	title = {The nuclear hormone receptor Ftz-F1 is a cofactor for the Drosophila homeodomain protein Ftz.},
	journal = {Nature},
	volume = {385},
	number = {6616},
	year = {1997},
	month = {1997 Feb 6},
	pages = {552-5},
	abstract = {
	Homeobox genes specify cell fate and positional identity in embryos throughout the animal kingdom. Paradoxically, although each has a specific function in vivo, the in vitro DNA-binding specificities of homeodomain proteins are overlapping and relatively weak. A current model is that homeodomain proteins interact with cofactors that increase specificity in vivo. Here we use a native binding site for the homeodomain protein Fushi tarazu (Ftz) to isolate Ftz-F1, a protein of the nuclear hormone-receptor superfamily and a new Ftz cofactor. Ftz and Ftz-F1 are present in a complex in Drosophila embryos. Ftz-F1 facilitates the binding of Ftz to DNA, allowing interactions with weak-affinity sites at concentrations of Ftz that alone bind only high-affinity sites. Embryos lacking Ftz-F1 display ftz-like pair-rule cuticular defects. This phenotype is a result of abnormal ftz function because it is expressed but fails to activate downstream target genes. Cooperative interaction between homeodomain proteins and cofactors of different classes may serve as a general mechanism to increase HOX protein specificity and to broaden the range of target sites they regulate.

},
	keywords = {Animals, Base Sequence, Binding Sites, Cloning, Molecular, DNA, DNA-Binding Proteins, Drosophila, Drosophila Proteins, Female, Fushi Tarazu Transcription Factors, Gene Expression Regulation, Developmental, Homeodomain Proteins, Insect Proteins, Male, Molecular Sequence Data, Mutation, Protein Binding, Receptors, Cytoplasmic and Nuclear, Saccharomyces cerevisiae, Steroidogenic Factor 1, Transcription Factors},
	issn = {0028-0836},
	doi = {10.1038/385552a0},
	author = {Yu, Y. and W Li and Su, K and Yussa, M and Han, W. and Perrimon, N and Pick, L}
}
