Nucleic Acids Research Advance Access originally published online on October 26, 2006
Nucleic Acids Research 2006 34(20):5951-5965; doi:10.1093/nar/gkl689
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Nucleic Acids Research, 2006, Vol. 34, No. 20 5951-5965
© 2006 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Molecular Biology |
Functional interactions between Dlx2 and lymphoid enhancer factor regulate Msx2
Center for Environmental and Genetic Medicine, Institute of Biosciences and Genetic Medicine Texas A&M Health Science Center, 2121 W. Holcombe Boulevard, Houston, TX 77030, USA
*To whom correspondence should be addressed. Tel: +1 713 677 7402; Fax: +1 713 677 7784; Email: bamendt{at}ibt.tamhsc.edu
Received May 26, 2006. Revised September 7, 2006. Accepted September 7, 2006.
Dlx2, Lymphoid Enhancer Factor (Lef-1) and Msx2 transcription factors are required for several developmental processes. To understand the control of gene expression by these factors, chromatin immunoprecipitation (ChIP) assays identified Msx2 as a downstream target of Dlx2 and Lef-1. Dlx2 activates the Msx2 promoter in several cell lines and binds DNA as a monomer and dimer. A Lef-1 ß-catenin-dependent isoform minimally activates the Msx2 promoter and a Lef-1 ß-catenin-independent isoform is inactive, however co-expression of Dlx2 and both Lef-1 isoforms synergistically activate the Msx2 promoter. Co-immunoprecipitation and protein pull-down experiments demonstrate Lef-1 physically interacts with Dlx2. Deletion analyses of the Lef-1 protein reveal specific regions required for synergism with Dlx2. The Lef-1 ß-catenin binding domain (ßDB) is not required for its interaction with Dlx2. Msx2 can auto-regulate its promoter and repress Dlx2 activation. Msx2 repression of Dlx2 activation is dose-specific and both bind a common DNA-binding element. These transcriptional mechanisms correlate with the temporal and spatial expression of these factors and may provide a mechanism for the control of several developmental processes. We demonstrate new transcriptional activities for Dlx2, Msx2 and Lef-1 through protein interactions and identification of downstream targets.
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