Methylcytosine dioxygenase TET3 interacts with thyroid hormone nuclear receptors and stabilizes their association to chromatin
Open accessAbstract
Significance: Thyroid hormone (T3) controls both developmental and physiological processes. Its nuclear receptors (TR) are transcription factors. Methyl dioxygenase ten-eleven translocation protein 3 (TET3) is characterized here as a TR coregulator. It stabilizes and promotes TR chromatin association in a dioxygenase-independent manner, thus increasing the sensitivity of the cell to T3. Mutations in TR cause the resistance to thyroid hormone syndrome (RTH) symptom, the severity of which varies with the particular mutation. Only some mutated TR can be stabilized by TET3. The availability of TET3 is therefore a parameter modulating TR activity, and its differential interaction with mutated TR might explain different severity of RTH. Furthermore, TET3 is likely to function as a general coregulator for nuclear receptors, as it enhances chromatin association of additional members of this superfamily.
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TET3 has known interactions with another nuclear receptor family member, TRα1.
“We focused on TET3 due to its high expression in hepatocytes (Fig. 5A and 5B) and its known interactions with another nuclear receptor family member, TRα1 (36).”
From Hepatocyte Nuclear Factor 4‐Alpha Is Essential for the Active Epigenetic State at Enhancers in Mouse Liver (2019) · cites this paper as [36]
TET3 is known to interact with other TFs.
“Here, we focused on TET3 because it is more highly expressed compared to other TETs in liver and is known to interact with other TFs (36).”
From Hepatocyte Nuclear Factor 4‐Alpha Is Essential for the Active Epigenetic State at Enhancers in Mouse Liver (2019) · cites this paper as [36]
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Cites
TET1 and hydroxymethylcytosine in transcription and DNA methylation fidelity
Williams, K., Christensen, J., Pedersen, M. T., Johansen, J. V., Cloos, P. A. C., Rappsilber, J., & Helin, K. (2011) · Nature · doi:10.1038/nature10066 · Cited by 1,021 · see citing works
A Mutation in the Thyroid Hormone Receptor Alpha Gene
Bochukova, E., Schoenmakers, N., Agostini, M., Schoenmakers, E., Rajanayagam, O., Keogh, J. M., Henning, E., Reinemund, J., Gevers, E., Sarri, M., et al. (2012) · New England Journal of Medicine · doi:10.1056/nejmoa1110296 · Cited by 379 · see citing works
A Novel Mutation in THRA Gene Associated With an Atypical Phenotype of Resistance to Thyroid Hormone
Espiard, S., Savagner, F., Flamant, F., Vlaeminck-Guillem, V., Guyot, R., Munier, M., d'Herbomez, M., Bourguet, W., Pinto, G., Rose, C., et al. (2015) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2015-1120 · Cited by 75 · see citing works
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Thakur, A., Wong, J. C. H., Wang, E. Y., Lotto, J., Kim, D., Cheng, J., Mingay, M., Cullum, R., Moudgil, V., Ahmed, N., et al. (2019) · Hepatology · doi:10.1002/hep.30631 · Cited by 75 · see citing works
“Thus, H3K27ac at HNF4A binding sites could be affected by interactions with other TFs. Alternatively, HNF4A, with or without other factors, could have a protective effect that disallows histone deacetylases to act.”
BackgroundInfluentialSelf-citation
- Authors
- Guan, W., Guyot, R., Samarut, J., Flamant, F., Wong, J., & Gauthier, K. C.
- Affiliations
- École Normale Supérieure de Lyon (FR)
- East China Normal University (CN)
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2017-07-17
- Volume
- 114
- Issue
- 31
- Pages
- 8229-8234
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC5547603
- OpenAlex
- W2735951677
- Cited by
- 32
- References
- 3
- Citations by year
- 2026: 2 · 2024: 3 · 2023: 5 · 2022: 6 · 2021: 4 · 2020: 6 · 2019: 3 · 2018: 2 · 2017: 1
- FWCI
- 2.60
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- Funders
- Ministry of Science and Technology of the People's Republic of China (2015CB910402)
- National Natural Science Foundation of China (81530078, 31571325)
- Agence Nationale de la Recherche (ANR-15-CE14-0011-01)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Keywords
- TET3, thyroid hormone receptor, thyroid hormone receptor alpha 1, nuclear receptors, protein-protein interaction, chromatin association, transcriptional activation, coregulators, DNA demethylation
- MeSH terms
- Chromatin, Gene Expression Regulation, Humans, Mutation, Nitriles, Receptors, Androgen, Thiazoles, Transcription, Genetic, Catalytic Domain, Thyroid Hormone Receptors alpha, Thyroid Hormone Receptors beta, Immunoprecipitation, Dioxygenases, Protein Interaction Domains and Motifs, Ubiquitination, HEK293 Cells
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