Thyroid hormone receptor gene knockouts.

The thyroid hormone receptor genes, TRalpha and TRbeta, differ in developmental expression and tissue distribution. TRbeta knockout mice have goiter, elevated thyroid hormone and TSH levels, and a functional auditory defect. In contrast, mice with TRalpha 1/alpha2 inactivation have thyroid hypoplasia, low serum thyroid hormone levels, growth arrest and delayed small intestine maturation. Mice with selective TRalpha1 inactivation have apparent normal growth and development, but have bradycardia and reduced body temperature. The dramatic differences between these mice with TRbeta and TRalpha gene inactivations indicate the differential function of these genes. The influence of these gene inactivations on thyroid-stimulating hormone regulation is central to the resulting phenotypes.