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Abstract:
Mice devoid of all TRs are viable, whereas Pax8(-/-)mice, which lack the follicular cells producing T-4 and T-3 in the thyroid gland, die during the first weeks of postnatal life. A precise comparison between the two types of mutants reveals that their phenotypes are similar, but the defects in spleen, bone, and small intestine are more pronounced in Pax(-/-) mice. This is interpreted as the result of a negative effect of the unliganded TR on thyroid hormone target genes expression in the Pax(-/-)mutants. Pax8(-/-) compound mutants can survive to adulthood, and the expression of target genes is partially restored. This demonstrates the importance of TR alpha aporeceptor activity in several aspects of postnatal development.
