Linked Life Data

11726557

Source:http://linkedlifedata.com/resource/pubmed/id/11726557

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pubmed-article:11726557pubmed:dateCreated2001-11-29lld:pubmed
pubmed-article:11726557pubmed:abstractTextDeletion of thyroid hormone receptor beta (TR beta), a ligand-dependent transcription factor encoded by the Thrb gene, causes deafness and thyroid hyperactivity in Thrb-null (Thrb(tm1/tm1)) mice and in a recessive form of the human syndrome of resistance to thyroid hormone. Here, we have determined that a targeted mutation (Thra(tm2)) in the related Thra gene, encoding thyroid hormone receptor alpha suppresses these phenotypes in mice. Thra encodes a TR alpha 1 receptor which is non-essential for hearing and a TR alpha 2 splice variant of unknown function that neither binds thyroid hormone nor transactivates. The Thra(tm2) mutation deletes TR alpha 2 and concomitantly causes overexpression of TR alpha 1 as a consequence of the exon structure of the gene. Thra(tm2/tm2) mice have normal auditory thresholds indicating that TR alpha 2 is dispensable for hearing, and have only marginally reduced thyroid activity. However, a potent function for the Thra(tm2) allele is revealed upon its introduction into Thrb(tm1/tm1) mice, where it suppresses the auditory and thyroid phenotypes caused by loss of TR beta. These findings reveal a novel modifying function for a Thra allele and suggest that increased expression of TR alpha 1 may substitute for the absence of TR beta. The TR isotypes generated by the distinct Thrb and Thra genes represent a small family of receptors that have diverged to mediate different physiological roles; however, the ability of changes in Thra expression to compensate for loss of Thrb indicates that many functions of these genes remain closely related.lld:pubmed
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pubmed-article:11726557pubmed:authorpubmed-author:NordströmKKlld:pubmed
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pubmed-article:11726557pubmed:year2001lld:pubmed
pubmed-article:11726557pubmed:articleTitleSuppression of the deafness and thyroid dysfunction in Thrb-null mice by an independent mutation in the Thra thyroid hormone receptor alpha gene.lld:pubmed
pubmed-article:11726557pubmed:affiliationDepartment of Human Genetics, Box 1498, Mount Sinai School of Medicine, 1425 Madison Avenue, New York, NY 10029, USA.lld:pubmed
pubmed-article:11726557pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:11726557pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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