In this issue of Developmental Cell, Waldron et al. (2016) identify an interaction between a master regulator of heart development, TBX5, and the NuRD complex and describe how mutations affecting the interaction may contribute to congenital heart disease. Furthermore, these interactions may have contributed to the evolution of cardiac septation.
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University of North Carolina McAllister Heart Institute, UNC-Chapel Hill, Chapel Hill, NC 27599, USA; Integrative Program for Biological & Genome Sciences, UNC-Chapel Hill, Chapel Hill, NC 27599, USA; Department of Genetics, UNC-Chapel Hill, Chapel Hill, NC 27599, USA; Lineberger Comprehensive Cancer Center, UNC-Chapel Hill, Chapel Hill, NC 27599, USA; Department of Biology, UNC-Chapel Hill, Chapel Hill, NC 27599, USA. Electronic address:
Human mutations in the cardiac transcription factor gene TBX5 cause congenital heart disease (CHD), although the underlying mechanism is unknown. We report characterization of the endogenous TBX5 cardiac interactome and demonstrate that TBX5, long considered a transcriptional activator, interacts biochemically and genetically with the nucleosome remodeling and deacetylase (NuRD) repressor complex. Incompatible gene programs are repressed by TBX5 in the developing heart.
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Skaggs School of Pharmacy and Pharmaceutical Sciences, Departments of Pharmacology and Medicine, University of California, San Diego, La Jolla, CA 92093, USA. Electronic address:
In this issue of Developmental Cell, Waldron et al. (2016) identify an interaction between a master regulator of heart development, TBX5, and the NuRD complex and describe how mutations affecting the interaction may contribute to congenital heart disease. Furthermore, these interactions may have contributed to the evolution of cardiac septation.
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