Auto-regulation of thyroid hormone receptor genes during metamorphosis: roles in apoptosis and cell proliferation.
Amphibian metamorphosis is an excellent model system for studying postembryonic development in vertebrates. It involves specific degeneration of larval cells through programmed cell death with apoptotic morphology and selective proliferation and differentiation of adult cell types. Thyroid hormone (T3) plays a causative role in this process and the effects of T3 is presumed to be mediated by T3 receptors (TRs). Studies in other systems have suggested that TRs function as heterodimers formed with RXRs (9-cis retinoic acid receptors) and require the presence of various cofactor in transcriptional activation and repression in the presence and absence of T3, respectively. The T3-induced transcriptional activation leads to chromatin remodeling which may involve some of the cofactors. Recent investigation on receptor expression has implicated a role of TRs in T3-induced apoptosis in larval tissues and proliferation of adult cell types. Functional studies in tadpoles and developing embryos have provide strong support for such a role and further demonstrate the importance of RXR in mediating the effect of T3.
Shi
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YB
Laboratory of Molecular Embryology, National Institute of Child Health and Human Development, Bethesda, MD 20892-5431, USA. Shi@helix.nih.gov
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Li
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Damjanovski
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D000818:Animals; D017209:Apoptosis; D002455:Cell Division / Q000502:physiology*; D018507:Gene Expression Regulation, Developmental; D006706:Homeostasis; D006801:Humans; D008675:Metamorphosis, Biological; D011988:Receptors, Thyroid Hormone / Q000235:genetics*
D011988:Receptors, Thyroid Hormone