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

Yan Yu, Willis Li, Kai Su, Miyuki Yussa, Wei Han, Norbert Perrimon, Leslie Pick

Research output: Contribution to journalArticlepeer-review

155 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)552-555
Number of pages4
JournalNature
Volume385
Issue number6616
DOIs
StatePublished - Feb 6 1997
Externally publishedYes

ASJC Scopus subject areas

  • General

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