Transcriptional activation by the thyroid hormone receptor through ligand-dependent receptor recruitment and chromatin remodelling

Lars Grøntved, Joshua J. Waterfall, Dong Wook Kim, Songjoon Baek, Myong-Hee Sung, Li Zhao, Jeong Won Park, Ronni Nielsen, Robert L. Walker, Yuelin J. Zhu, Paul S. Meltzer, Gordon L. Hager and Sheue-yann Cheng ()
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Lars Grøntved: Laboratory of Receptor Biology and Gene Expression, Center for Cancer Research (CCR), National Cancer Institute (NCI), National Institutes of Health (NIH)
Joshua J. Waterfall: Genetics Branch, CCR, NCI, NIH
Dong Wook Kim: Laboratory of Molecular Biology, CCR, NCI, NIH, Building 37/NIH, Bethesda, Maryland 20892, USA
Songjoon Baek: Laboratory of Receptor Biology and Gene Expression, Center for Cancer Research (CCR), National Cancer Institute (NCI), National Institutes of Health (NIH)
Myong-Hee Sung: Laboratory of Receptor Biology and Gene Expression, Center for Cancer Research (CCR), National Cancer Institute (NCI), National Institutes of Health (NIH)
Li Zhao: Laboratory of Molecular Biology, CCR, NCI, NIH, Building 37/NIH, Bethesda, Maryland 20892, USA
Jeong Won Park: Laboratory of Molecular Biology, CCR, NCI, NIH, Building 37/NIH, Bethesda, Maryland 20892, USA
Ronni Nielsen: University of Southern Denmark
Robert L. Walker: Genetics Branch, CCR, NCI, NIH
Yuelin J. Zhu: Genetics Branch, CCR, NCI, NIH
Paul S. Meltzer: Genetics Branch, CCR, NCI, NIH
Gordon L. Hager: Laboratory of Receptor Biology and Gene Expression, Center for Cancer Research (CCR), National Cancer Institute (NCI), National Institutes of Health (NIH)
Sheue-yann Cheng: Laboratory of Molecular Biology, CCR, NCI, NIH, Building 37/NIH, Bethesda, Maryland 20892, USA

Nature Communications, 2015, vol. 6, issue 1, 1-11

Abstract: Abstract A bimodal switch model is widely used to describe transcriptional regulation by the thyroid hormone receptor (TR). In this model, the unliganded TR forms stable, chromatin-bound complexes with transcriptional co-repressors to repress transcription. Binding of hormone dissociates co-repressors and facilitates recruitment of co-activators to activate transcription. Here we show that in addition to hormone-independent TR occupancy, ChIP-seq against endogenous TR in mouse liver tissue demonstrates considerable hormone-induced TR recruitment to chromatin associated with chromatin remodelling and activated gene transcription. Genome-wide footprinting analysis using DNase-seq provides little evidence for TR footprints both in the absence and presence of hormone, suggesting that unliganded TR engagement with repressive complexes on chromatin is, similar to activating receptor complexes, a highly dynamic process. This dynamic and ligand-dependent interaction with chromatin is likely shared by all steroid hormone receptors regardless of their capacity to repress transcription in the absence of ligand.

Date: 2015
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DOI: 10.1038/ncomms8048

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