PROLACTIN PREVENTS THE AUTOINDUCTION OF THYROID-HORMONE RECEPTOR MESSENGER-RNAS DURING AMPHIBIAN METAMORPHOSIS

We have recently reported that prolactin (PRL) inhibits both morphogenesis and cell death in thyroid hormone (Ts)-induced amphibian metamorphosis (Tata et al., 1991), and that the autoinduction of T3 receptor (TR α and β) mRNA is among the most rapid responses of premetamorphic Xenopus tadpoles to T3 (Kawahara et al., 1991). We now demonstrate that PRL prevents the rapid T3-induced upregulation of TR α and β mRNAs in stages 50-54 Xenopus tadpoles and in organ cultures of tadpole tails. This effect is followed by the inhibition of the de novo activation of 63-kDa keratin gene by T3. We present an experimentally testable model whereby PRL exerts its juvenilizing action by preventing the amplification of TR by its autoinduction by T3. © 1992.