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In the 'template-engaged' form activity of RNA polymerase I in nuclei of normal rat livers, about 40% of the activity was found to be influenced by thyroid hormones and glucocorticoids and can be eliminated by 1 h treatment with cycloheximide. On the other hand, the 'free' form activity of the enzyme in rat liver nuclei and the total amount of the enzyme in nucleoli were scarcely affected by these hormones. These results suggest that a considerable portion of rRNA synthesis in rat liver nucleoli is regulated by the initiation of rDNA transcription, probably with the participation of glucocorticoid- and thyroid hormone-dependent short-lived protein(s). When somatotropin, in addition to glucocorticoids and thyroid hormones, was depleted by hypophysectomy, the 'template-engaged' form activity of RNA polymerase I was reduced to 30% of the normal level. The activity was restored completely by a single injection of triiodothyronine plus somatotropin, but not by injections of the individual hormones. From these results, it is likely that the stimulating effects of glucocorticoids and thyroid hormones on rRNA synthesis are maintained by the action of somatotropin which seems to occur in a different mechanism from those of the former two hormones. In contrast to these hormones, androgen showed no acute effect on 'template-engaged' form activity of RNA polymerase I in liver nuclei.

In Vivo Effects of Thyroid Hormone, Glucocorticoid, Androgen, and Somatotropin on RNA Polymerase I Activities in Isolated Liver Nuclei.