Life Without Thyroid Hormone Receptor

Thyroid hormone (T3) is critical not only for organ function and metabolism in the adult but also for animal development. This is particularly true during the neonatal period when T3 levels are high in mammals. Many processes during this postembryonic developmental period resemble those during amphi...

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Published inEndocrinology (Philadelphia) Vol. 162; no. 4; p. 1
Main Author Shi, Yun-Bo
Format Journal Article
LanguageEnglish
Published US Oxford University Press 01.04.2021
Subjects
Amphibians
Analysis
Animals
Degeneration
Diploids
Divergence
Endocrinology
Frogs
Gene Expression Regulation, Developmental
Gene silencing
Genes
Genetic modification
Genome editing
Hormones
Humans
Lethality
Mammals
Mammals - genetics
Mammals - growth & development
Mammals - metabolism
Metabolism
Metamorphosis
Metamorphosis, Biological
Mini-Reviews
Neonates
Organs
Receptors
Receptors, Thyroid Hormone - genetics
Receptors, Thyroid Hormone - metabolism
Thyroid
Thyroid gland
Tissues
Triiodothyronine
Triiodothyronine - metabolism
Vertebrates
amphibian metamorphosis
thyroid hormone receptor
histone modification
adult stem cells
Xenopus tropicalis
Xenopus laevis
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Abstract Thyroid hormone (T3) is critical not only for organ function and metabolism in the adult but also for animal development. This is particularly true during the neonatal period when T3 levels are high in mammals. Many processes during this postembryonic developmental period resemble those during amphibian metamorphosis. Anuran metamorphosis is perhaps the most dramatic developmental process controlled by T3 and affects essentially all organs/tissues, often in an organ autonomous manner. This offers a unique opportunity to study how T3 regulates vertebrate development. Earlier transgenic studies in the pseudo-tetraploid anuran Xenopus laevis revealed that T3 receptors (TRs) are necessary and sufficient for mediating the effects of T3 during metamorphosis. Recent gene knockout studies with gene-editing technologies in the highly related diploid anuran Xenopus tropicalis showed, surprisingly, that TRs are not required for most metamorphic transformations, although tadpoles lacking TRs are stalled at the climax of metamorphosis and eventually die. Analyses of the changes in different organs suggest that removal of TRs enables premature development of many adult tissues, likely due to de-repression of T3-inducible genes, while preventing the degeneration of tadpole-specific tissues, which is possibly responsible for the eventual lethality. Comparison with findings in TR knockout mice suggests both conservation and divergence in TR functions, with the latter likely due to the greatly reduced need, if any, to remove embryo/prenatal-specific tissues during mammalian postembryonic development.
AbstractList Thyroid hormone (T3) is critical not only for organ function and metabolism in the adult but also for animal development. This is particularly true during the neonatal period when T3 levels are high in mammals. Many processes during this postembryonic developmental period resemble those during amphibian metamorphosis. Anuran metamorphosis is perhaps the most dramatic developmental process controlled by T3 and affects essentially all organs/tissues, often in an organ autonomous manner. This offers a unique opportunity to study how T3 regulates vertebrate development. Earlier transgenic studies in the pseudo-tetraploid anuran Xenopus laevis revealed that T3 receptors (TRs) are necessary and sufficient for mediating the effects of T3 during metamorphosis. Recent gene knockout studies with gene-editing technologies in the highly related diploid anuran Xenopus tropicalis showed, surprisingly, that TRs are not required for most metamorphic transformations, although tadpoles lacking TRs are stalled at the climax of metamorphosis and eventually die. Analyses of the changes in different organs suggest that removal of TRs enables premature development of many adult tissues, likely due to de-repression of T3-inducible genes, while preventing the degeneration of tadpole-specific tissues, which is possibly responsible for the eventual lethality. Comparison with findings in TR knockout mice suggests both conservation and divergence in TR functions, with the latter likely due to the greatly reduced need, if any, to remove embryo/prenatal-specific tissues during mammalian postembryonic development.
Thyroid hormone (T3) is critical not only for organ function and metabolism in the adult but also for animal development. This is particularly true during the neonatal period when T3 levels are high in mammals. Many processes during this postembryonic developmental period resemble those during amphibian metamorphosis. Anuran metamorphosis is perhaps the most dramatic developmental process controlled by T3 and affects essentially all organs/tissues, often in an organ autonomous manner. This offers a unique opportunity to study how T3 regulates vertebrate development. Earlier trans-genic studies in the pseudo-tetraploid anuran Xenopus laevis revealed that T3 receptors (TRs) are necessary and sufficient for mediating the effects ofT3 during metamorphosis. Recent gene knockout studies with gene-editing technologies in the highly related dip-loid anuran Xenopus tropicalis showed, surprisingly, that TRs are not required for most metamorphic transformations, although tadpoles lacking TRs are stalled at the climax of metamorphosis and eventually die. Analyses of the changes in different organs suggest that removal of TRs enables premature development of many adult tissues, likely due to de-repression of T3-inducible genes, while preventing the degeneration of tadpole-specific tissues, which is possibly responsible for the eventual lethality. Comparison with findings inTR knockout mice suggests both conservation and divergence inTR functions, with the latter likely due to the greatly reduced need, if any, to remove embryo/prenatal-specific tissues during mammalian postembryonic development. Key Words: amphibian metamorphosis, Xenopus laevis, Xenopus tropicalis, thyroid hormone receptor, adult stem cells, histone modification
Thyroid hormone (T3) is critical not only for organ function and metabolism in the adult but also for animal development. This is particularly true during the neonatal period when T3 levels are high in mammals. Many processes during this postembryonic developmental period resemble those during amphibian metamorphosis. Anuran metamorphosis is perhaps the most dramatic developmental process controlled by T3 and affects essentially all organs/tissues, often in an organ autonomous manner. This offers a unique opportunity to study how T3 regulates vertebrate development. Earlier trans-genic studies in the pseudo-tetraploid anuran Xenopus laevis revealed that T3 receptors (TRs) are necessary and sufficient for mediating the effects ofT3 during metamorphosis. Recent gene knockout studies with gene-editing technologies in the highly related dip-loid anuran Xenopus tropicalis showed, surprisingly, that TRs are not required for most metamorphic transformations, although tadpoles lacking TRs are stalled at the climax of metamorphosis and eventually die. Analyses of the changes in different organs suggest that removal of TRs enables premature development of many adult tissues, likely due to de-repression of T3-inducible genes, while preventing the degeneration of tadpole-specific tissues, which is possibly responsible for the eventual lethality. Comparison with findings inTR knockout mice suggests both conservation and divergence inTR functions, with the latter likely due to the greatly reduced need, if any, to remove embryo/prenatal-specific tissues during mammalian postembryonic development.
Thyroid hormone (T3) is critical not only for organ function and metabolism in the adult but also for animal development. This is particularly true during the neonatal period when T3 levels are high in mammals. Many processes during this postembryonic developmental period resemble those during amphibian metamorphosis. Anuran metamorphosis is perhaps the most dramatic developmental process controlled by T3 and affects essentially all organs/tissues, often in an organ autonomous manner. This offers a unique opportunity to study how T3 regulates vertebrate development. Earlier transgenic studies in the pseudo-tetraploid anuran Xenopus laevis revealed that T3 receptors (TRs) are necessary and sufficient for mediating the effects of T3 during metamorphosis. Recent gene knockout studies with gene-editing technologies in the highly related diploid anuran Xenopus tropicalis showed, surprisingly, that TRs are not required for most metamorphic transformations, although tadpoles lacking TRs are stalled at the climax of metamorphosis and eventually die. Analyses of the changes in different organs suggest that removal of TRs enables premature development of many adult tissues, likely due to de-repression of T3-inducible genes, while preventing the degeneration of tadpole-specific tissues, which is possibly responsible for the eventual lethality. Comparison with findings in TR knockout mice suggests both conservation and divergence in TR functions, with the latter likely due to the greatly reduced need, if any, to remove embryo/prenatal-specific tissues during mammalian postembryonic development.Thyroid hormone (T3) is critical not only for organ function and metabolism in the adult but also for animal development. This is particularly true during the neonatal period when T3 levels are high in mammals. Many processes during this postembryonic developmental period resemble those during amphibian metamorphosis. Anuran metamorphosis is perhaps the most dramatic developmental process controlled by T3 and affects essentially all organs/tissues, often in an organ autonomous manner. This offers a unique opportunity to study how T3 regulates vertebrate development. Earlier transgenic studies in the pseudo-tetraploid anuran Xenopus laevis revealed that T3 receptors (TRs) are necessary and sufficient for mediating the effects of T3 during metamorphosis. Recent gene knockout studies with gene-editing technologies in the highly related diploid anuran Xenopus tropicalis showed, surprisingly, that TRs are not required for most metamorphic transformations, although tadpoles lacking TRs are stalled at the climax of metamorphosis and eventually die. Analyses of the changes in different organs suggest that removal of TRs enables premature development of many adult tissues, likely due to de-repression of T3-inducible genes, while preventing the degeneration of tadpole-specific tissues, which is possibly responsible for the eventual lethality. Comparison with findings in TR knockout mice suggests both conservation and divergence in TR functions, with the latter likely due to the greatly reduced need, if any, to remove embryo/prenatal-specific tissues during mammalian postembryonic development.
Thyroid hormone (T3) is critical not only for organ function and metabolism in the adult but also for animal development. This is particularly true during the neonatal period when T3 levels are high in mammals. Many processes during this postembryonic developmental period resemble those during amphibian metamorphosis. Anuran metamorphosis is perhaps the most dramatic developmental process controlled by T3 and affects essentially all organs/tissues, often in an organ autonomous manner. This offers a unique opportunity to study how T3 regulates vertebrate development. Earlier transgenic studies in the pseudo-tetraploid anuran Xenopus laevis revealed that T3 receptors (TRs) are necessary and sufficient for mediating the effects of T3 during metamorphosis. Recent gene knockout studies with gene-editing technologies in the highly related diploid anuran Xenopus tropicalis showed, surprisingly, that TRs are not required for most metamorphic transformations, although tadpoles lacking TRs are stalled at the climax of metamorphosis and eventually die. Analyses of the changes in different organs suggest that removal of TRs enables premature development of many adult tissues, likely due to de-repression of T3-inducible genes, while preventing the degeneration of tadpole-specific tissues, which is possibly responsible for the eventual lethality. Comparison with findings in TR knockout mice suggests both conservation and divergence in TR functions, with the latter likely due to the greatly reduced need, if any, to remove embryo/prenatal-specific tissues during mammalian postembryonic development.
Audience Academic
Author Shi, Yun-Bo
AuthorAffiliation Section on Molecular Morphogenesis, National Institute of Child Health and Human Development, National Institutes of Health , Bethesda, MD, USA
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  organization: Section on Molecular Morphogenesis, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, USA
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Issue 4
Keywords amphibian metamorphosis
thyroid hormone receptor
histone modification
adult stem cells
Xenopus tropicalis
Xenopus laevis
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PublicationPlace_xml – name: US
– name: United States
– name: Washington
PublicationTitle Endocrinology (Philadelphia)
PublicationTitleAlternate Endocrinology
PublicationYear 2021
Publisher Oxford University Press
Publisher_xml – name: Oxford University Press
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SecondaryResourceType review_article
Snippet Thyroid hormone (T3) is critical not only for organ function and metabolism in the adult but also for animal development. This is particularly true during the...
SourceID pubmedcentral
proquest
gale
pubmed
crossref
oup
SourceType Open Access Repository
Aggregation Database
Index Database
Enrichment Source
Publisher
StartPage 1
SubjectTerms Amphibians
Analysis
Animals
Degeneration
Diploids
Divergence
Endocrinology
Frogs
Gene Expression Regulation, Developmental
Gene silencing
Genes
Genetic modification
Genome editing
Hormones
Humans
Lethality
Mammals
Mammals - genetics
Mammals - growth & development
Mammals - metabolism
Metabolism
Metamorphosis
Metamorphosis, Biological
Mini-Reviews
Neonates
Organs
Receptors
Receptors, Thyroid Hormone - genetics
Receptors, Thyroid Hormone - metabolism
Thyroid
Thyroid gland
Tissues
Triiodothyronine
Triiodothyronine - metabolism
Vertebrates
Title Life Without Thyroid Hormone Receptor
URI https://www.ncbi.nlm.nih.gov/pubmed/33558878
https://www.proquest.com/docview/2891656016
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Volume 162
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