Targeted remodeling of human beta-globin promoter chromatin structure produces increased expression and decreased silencing.

The chromatin structure of the human beta-globin gene locus assumes a transcriptionally-active conformation in erythroid cells. One feature of this chromatin reorganization is the formation of DNase 1 hypersensitive sites in the regions of active globin gene promoters. This reorganization requires the globin locus control region and is associated with normal expression of the beta-like globin genes.

Heterodimerization of Msx and Dlx homeoproteins results in functional antagonism.

Protein-protein interactions are known to be essential for specifying the transcriptional activities of homeoproteins. Here we show that representative members of the Msx and Dlx homeoprotein families form homo- and heterodimeric complexes. We demonstrate that dimerization by Msx and Dlx proteins is mediated through their homeodomains and that the residues required for this interaction correspond to those necessary for DNA binding.

Rapid identification of homeodomain binding sites in the Wnt-5a gene using an immunoprecipitation strategy.

Here we describe an immunoprecipitation approach for identifying homeodomain binding sites within uncharacterized genomic sequences of a putative downstream target gene, Wnt-5a. Immunoprecipitation of Wnt-5a genomic fragments was performed using a purified Msx1 homeodomain polypeptide (Msx1) and its corresponding antisera (alpha-Msx1). This resulted in isolation of three fragments containing multiple DNA binding sites for Msx1, as confirmed by DNA binding studies.

A single homeodomain binding site restricts spatial expression of Wnt-1 in the developing brain.

In this study we investigate the molecular mechanisms that are responsible for the restricted expression of Wnt-1 during embryogenesis. We report that a single homeodomain binding site, HBS1, within the Wnt-1 enhancer contributes to appropriate spatial expression of Wnt-1 in the developing nervous system. This HBS1 site may be required for repressing Wnt-1 expression in the developing forebrain since specific mutations of this site result in an extension of the rostral boundary of Wnt-1/lacZ staining in transgenic embryos.