title: Multiple thyroid hormone-induced muscle growth and death programs during metamorphosis in Xenopus laevis.
abstract: Xenopus laevis tadpole tails contain fast muscle fibers oriented in chevrons and two pairs of slow muscle "cords" along the length of the tail. When tail resorption is inhibited by a number of different treatments, fast muscle but not the slow cord muscle still is lost, demonstrating that the fast tail muscle is a direct target of the thyroid hormone-induced death program. Expression of a dominant negative form of the thyroid hormone receptor (TRDNalpha) was restricted to tadpole muscle by means of a muscle-specific promoter. Even though the transgene protects fast tail muscle from thyroid hormone (TH)-induced death, the tail shortens, and the distal muscle chevrons at the tail tip are degraded. This default pathway for muscle death is probably caused by the action of proteolytic enzymes secreted by neighboring fibroblasts. Non-muscle tissues that are sensitive to TH, such as the fibroblasts, are not protected by the transgene when it is expressed solely in muscle. If allowed to develop to metamorphosis, these transgenic animals die at the climax of metamorphosis before tail resorption has begun. Their limbs have very little muscle even though the rest of limb morphology is normal. Thus, fast tail muscle and limb muscle have their own cell autonomous death and growth programs, respectively, that are independent of the fate of the other neighboring cell types. In contrast, death of the slow muscle is controlled by the other cell types of the tail.
authors.affiliation: Department of Embryology, Carnegie Institution of Washington, 115 West University Parkway, Baltimore, MD 21210, USA.
authors.forename: Biswajit
authors.initials: B
authors.lastname: Das
authors.forename: Alexander M
authors.initials: AM
authors.lastname: Schreiber
authors.forename: Haochu
authors.initials: H
authors.lastname: Huang
authors.forename: Donald D
authors.initials: DD
authors.lastname: Brown
mesh_terms: D000818:Animals; D030801:Animals, Genetically Modified; D017209:Apoptosis / Q000187:drug effects; D053148:Caspase 3; D020169:Caspases / Q000378:metabolism; D004789:Enzyme Activation; D015870:Gene Expression; D018507:Gene Expression Regulation, Developmental / Q000187:drug effects; D049452:Green Fluorescent Proteins; D007814:Larva / Q000187:drug effects / Q000254:growth & development / Q000378:metabolism; D008164:Luminescent Proteins / Q000235:genetics / Q000378:metabolism; D008675:Metamorphosis, Biological; D018482:Muscle, Skeletal / Q000166:cytology / Q000187:drug effects* / Q000254:growth & development* / Q000378:metabolism; D011401:Promoter Regions, Genetic; D011988:Receptors, Thyroid Hormone / Q000235:genetics / Q000378:metabolism; D011994:Recombinant Proteins / Q000235:genetics / Q000378:metabolism; D013963:Thyroid Hormones / Q000494:pharmacology*; D014982:Xenopus laevis / Q000235:genetics / Q000254:growth & development*
chemical_list: D008164:Luminescent Proteins; D011988:Receptors, Thyroid Hormone; D011994:Recombinant Proteins; D013963:Thyroid Hormones; D049452:Green Fluorescent Proteins; D053148:Caspase 3; D020169:Caspases