ArticlePLoS genetics2020
Multiple mechanisms regulate H3 acetylation of enhancers in response to thyroid hormone.
Article in PLoS genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 34 citations in OpenAlex.
- Dynamic regulation of H3K9 modifications in cancer: pathogenesis and targeted therapies.Biomarker research · 2026Review
- The human THRB thyroid hormone receptor gene and the puzzle of retinal disease phenotypes.Developmental biology · 2026Review
- Nuclear receptor coregulator interactions: beyond the switch.Genes & development · 2026Review
- RNA-seq and ChIP-seq unveils thyroid hormone receptor α deficiency affects skeletal muscle myoblast proliferation and differentiation via Col6a1 during aging.Journal of muscle research and cell motility · 2025Article
- NAL1 forms a molecular cage to regulate FZP phase separation.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Repeated fasting events sensitize enhancers, transcription factor activity and gene expression to support augmented ketogenesis.Nucleic acids research · 2025Article
- Thyroid Hormone Action by Genomic and Nongenomic Molecular Mechanisms.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Actions of thyroid hormones and thyromimetics on the liver.Nature reviews. Gastroenterology & hepatology · 2025Review
- Nuclear receptor corepressor 1 levels differentially impact the intracellular dynamics of mutant thyroid hormone receptors associated with resistance to thyroid hormone syndrome.Molecular and cellular endocrinology · 2024Article
- TRβ activation confers AT2-to-AT1 cell differentiation and anti-fibrosis during lung repair via KLF2 and CEBPA.Nature communications · 2024Article
- LXR-dependent enhancer activation regulates the temporal organization of the liver's response to refeeding leading to lipogenic gene overshoot.PLoS biology · 2024Article
- Thyroid hormone-regulated chromatin landscape and transcriptional sensitivity of the pituitary gland.Communications biology · 2023Article
- International Union of Basic and Clinical Pharmacology CXIII: Nuclear Receptor Superfamily-Update 2023.Pharmacological reviews · 2023Review
- Hepatic thyroid hormone signalling modulates glucose homeostasis through the regulation of GLP-1 production via bile acid-mediated FXR antagonism.Nature communications · 2022Article
- An Atlas of Thyroid Hormone Receptors' Target Genes in Mouse Tissues.International journal of molecular sciences · 2022Article
- Hormone-controlled cooperative binding of transcription factors drives synergistic induction of fasting-regulated genes.Nucleic acids research · 2022Article
- Thyroid hormone dependent transcriptional programming by TRβ requires SWI/SNF chromatin remodelers.Nucleic acids research · 2022Article
- Phase separation in transcription factor dynamics and chromatin organization.Current opinion in structural biology · 2021Review
- Neonatal thyroxine activation modifies epigenetic programming of the liver.Nature communications · 2021Article
- A coregulator shift, rather than the canonical switch, underlies thyroid hormone action in the liver.Genes & development · 2021Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
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Abstract
Hormone-dependent activation of enhancers includes histone hyperacetylation and mediator recruitment. Histone hyperacetylation is mostly explained by a bimodal switch model, where histone deacetylases (HDACs) disassociate from chromatin, and histone acetyl transferases (HATs) are recruited. This model builds on decades of research on steroid receptor regulation of transcription. Yet, the general concept of the bimodal switch model has not been rigorously tested genome wide. We have used a genomics approach to study enhancer hyperacetylation by the thyroid hormone receptor (TR), described to operate as a bimodal switch. H3 acetylation, HAT and HDAC ChIP-seq analyses of livers from hypo- and hyperthyroid wildtype, TR deficient and NCOR1 disrupted mice reveal three types of thyroid hormone (T3)-regulated enhancers. One subset of enhancers is bound by HDAC3-NCOR1 in the absence of hormone and constitutively occupy TR and HATs irrespective of T3 levels, suggesting a poised enhancer state in absence of hormone. In presence of T3, HDAC3-NCOR1 dissociates from these enhancers leading to histone hyperacetylation, suggesting a histone acetylation rheostat function of HDACs at poised enhancers. Another subset of enhancers, not occupied by HDACs, is hyperacetylated in a T3-dependent manner, where TR is recruited to chromatin together with HATs. Lastly, a subset of enhancers, is not occupied directly by TR yet requires TR for histone hyperacetylation. This indirect enhancer activation involves co-association with TR bound enhancers within super-enhancers or topological associated domains. Collectively, this demonstrates various mechanisms controlling hormone-dependent transcription and adds significant details to the otherwise simple bimodal switch model.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.