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The nuclear hormone receptor Ftz-F1 is a cofactor for the Drosophila homeodomain protein Ftz

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Abstract

Homeobox genes specify cell fate and positional identity in embryos throughout the animal kingdom1. 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 vivo2,3. Here we use a native binding site for the homeodomain protein Fushi tarazu (Ftz) to isolate Ftz-Fl, a protein of the nuclear hormone-receptor superfamily and a new Ftz cofactor. Ftz and Ftz-Fl are present in a complex in Drosophila embryos. Ftz-Fl 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-Fl 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.

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Authors and Affiliations

  1. Brookdale Center for Molecular Biology, Mount Sinai School of Medicine, One Gustave L Levy Place, New York, New York, 10029, USA

    Yan Yu, Kai Su, Miyuki Yussa, Wei Han & Leslie Pick

  2. Howard Hughes Medical Institute, Department of Genetics, Harvard Medical School, 200 Longwood Avenue, Boston, Massachusetts, 02115, USA

    Willis Li & Norbert Perrimon

Authors
  1. Yan Yu
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  2. Willis Li
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  3. Kai Su
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  4. Miyuki Yussa
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  5. Wei Han
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  6. Norbert Perrimon
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  7. Leslie Pick
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Yu, Y., Li, W., Su, K. et al. The nuclear hormone receptor Ftz-F1 is a cofactor for the Drosophila homeodomain protein Ftz. Nature 385, 552–555 (1997). https://doi.org/10.1038/385552a0

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