UTX, a histone H3-lysine 27 demethylase, acts as a critical switch to activate the cardiac developmental program.

The removal of histone H3 lysine27 (H3K27) trimethylation mark is important for the robust induction of many cell type-specific genes during differentiation. Here we show that UTX, a H3K27 demethylase, acts as a critical switch to promote a cardiac-specific gene program. UTX-deficient ESCs failed to develop heart-like rhythmic contractions under ...
a cardiac differentiation condition. UTX-deficient mice show severe defects in heart development and embryonic lethality. We found that UTX is recruited to cardiac-specific enhancers by associating with core cardiac transcription factors and demethylates H3K27 residues in cardiac genes. In addition, UTX facilitates the recruitment of Brg1 to the cardiac-specific enhancers. Together, our data reveal key roles for UTX in a timely transition from poised to active chromatin in cardiac genes during heart development and a fundamental mechanism by which a H3K27 demethylase triggers tissue-specific chromatin changes.
Mesh Terms:
Animals, Apoptosis, Blotting, Western, Cell Differentiation, Cell Lineage, Cell Proliferation, Chromatin, Chromatin Immunoprecipitation, DNA Helicases, Embryonic Stem Cells, Enhancer Elements, Genetic, Flow Cytometry, Genes, Lethal, Heart, Histones, Immunoenzyme Techniques, Luciferases, Methylation, Mice, Mice, Knockout, Nuclear Proteins, RNA, Messenger, Real-Time Polymerase Chain Reaction, Transcription Factors
Dev. Cell
Date: Jan. 17, 2012
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