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MBC in Press, published online ahead of print February 6, 2004
Mol. Biol. Cell 10.1091/mbc.E03-09-0636

A more recent version of this article appeared on April 1, 2004
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Submitted on September 2, 2003
Revised on December 19, 2003
Accepted on December 20, 2003

Cell cycle-dependent expression of thyroid hormone receptor-{beta} is a mechanism for variable hormone sensitivity

Padma Maruvada1, Natalia I Dmitrieva2, Joyce East-Palmer1, and Paul M Yen1

1 Molecular Regulation and Neuroendocrinology Section, Clinical Endocrinology Branch, National Institute of Diabetes, Digestive, and Kidney Diseases, National Institutes of Health, Bethesda, MD, 20892
2 Molecular Regulation and Neuroendocrinology Section, Clinical Endocrinology Branch, National Institute of Diabetes, Digestive, and Kidney Diseases, and Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, 20892

Thyroid hormone receptors (TRs) are ligand-regulatable transcription factors. Currently, little is known about the expression of TRs or other nuclear hormone receptors (NRs) during the cell cycle. We thus developed a stable expression system to express GFP-TR{beta} in HeLa cells under tetracycline regulation, and studied TR expression during the cell cycle by laser scanning cytometry (LSC). Only ~9-15% of the nonsynchronized cell population expressed TR as the majority of cells were in G1 phase and did not express detectable amounts of TR. However, when cells were synchronized in early S-phase with hydroxyurea and then released, TR expression levels increased in a cell cycle-dependent manner, and peaked to 30-40% cells expressing TR at late G2/M phase before declining to nonsynchronized levels. Moreover, we observed a direct correlation between transcriptional activity and TR expression during the cell cycle. Similar cell cycle-dependent findings also were observed for endogenous TR in rat pituitary GH3 cells. Last, cycloheximide studies demonstrated that the increase in TR expression was primarily due to increased translation. These novel observations of cell cycle-dependent expression of TR suggest that differential hormone sensitivity can occur during the cell cycle, and may contribute to cell cycle progression during normal development and oncogenesis.




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