The effects of oestradiol-17β on the ribonucleic acid polymerases of immature rabbit uterus

Abstract

Measurements of the endogenous RNA polymerase activities of nuclei isolated from immature rabbit uteri have shown that prior treatment of the animals with oestradiol-17beta has a profound effect on the apparent activities of both RNA polymerases A and B. Within 1 h of hormone treatment, the activity of RNA polymerase A is increased and continues to rise until about 4h when it reaches a plateau and remains steady until at least 8h. The activity of RNA polymerase B increases sharply after oestradiol treatment reaching an early maximum at 30-45 min. Thereafter this activity declines until by 1-2h it approaches control values but a second increase in activity then occurs with a maximum at 3-4h. Treatment of the rabbits with alpha-amanitin before the administration of oestradiol inhibits the hormone-induced stimulation of RNA polymerase A activity in isolated nuclei but when the administration of alpha-amanitin is delayed until after the early rise of RNA polymerase B activity, the oestradiol-induced stimulation of RNA polymerase A is retained. Similar results have been obtained in experiments with cycloheximide suggesting that the stimulation of RNA polymerase A activity by oestradiol is dependent on the hormone-induced stimulation of RNA polymerase B and the subsequent synthesis of protein using the RNA product of the early increase in RNA polymerase B activity. Measurement of the activities of RNA polymerases A and B after isolation of the enzymes from immature rabbit uterine nuclei before and after oestradiol treatment failed to show any differences. Therefore it would appear that the changes in the observed activities of RNA polymerases A and B in isolated nuclei are consequences of changes in the structure and function of chromatin rather than the results of modifications in the RNA polymerases themselves.

Steroid Receptors: Elements for Modulation of Eukaryotic Transcription

“…Although data concerning primary and secondary responses in mammals are less clear than in insects, similar amplification processes seem to occur in tissues where massive effects on growth and cell differentiation are observed (102,104; see also 103). Perhaps most striking is the fact that, as in Drosophila.…”

A Status Report – Human Prostatic Carcinoma, with Emphasis on Potential for Viral Etiology

“…Myeloblasts, pancreatic acinar cells and hen oviduct cells in fowl leukosis, and erythroblasts and megakaryocytes in mice are other examples wherein hormones may augment oncoviral proliferation. Whether hormones act on the surfaces of these cells or initiate their specific effect on transcriptional and/or translational phenomena within the cells [126][127][128], it is likely that expression of viruses, parti cularly those whose genomes are closely associated with cel lular DNA will be dramatically influenced by the hormonally stimulated state of the cell. Prostatic tissue, under direct hormonal control, may be a prime candidate for viral para sitism and expression.…”

Isolated uterine nuclei and cytosol receptors of aged rats exhibit impaired estrogenic stimulation of RNA polymerase II.

“…Although a number of other tissues exhibit similar loss of estrogen receptors and/or responsiveness during aging (11,12), several systems show no receptor loss despite altered hormonal sensitivity (5,(13)(14)(15) (15)(16)(17)(18). It has been shown previously that estrogenic stimulation of uterine RNA polymerase II (2) and total RNA synthesis (3) is reduced during aging in vivo.…”

“…Examples include reduced or delayed induction of phosphofructokinase (1), phosphohexose isomerase (1), and RNA polymerase 11 (2), as well as decreases in RNA synthesis (3), decidualization response (4), and weight maintainance (4). There is generally good agreement that this impaired responsiveness is at least partially due to loss of estrogen receptors (4-8, *) or reduced receptor translocation into nuclei in vivo (9, 10) during senescence.Although a number of other tissues exhibit similar loss of estrogen receptors and/or responsiveness during aging (11,12), several systems show no receptor loss despite altered hormonal sensitivity (5,(13)(14)(15) (15)(16)(17)(18). It has been shown previously that estrogenic stimulation of uterine RNA polymerase II (2) and total RNA synthesis (3) is reduced during aging in vivo.…”

“…Thus, it became important to examine various postreceptor events in aged uteri to determine whether or not they were independently affected by the aging process. Since most estrogen-dependent functions require transcription of specific mRNAs, stimulation of nuclear RNA polymerase II represents a critical event in the estrogenic signal transmission sequence (15)(16)(17)(18). It has been shown previously that estrogenic stimulation of uterine RNA polymerase II (2) and total RNA synthesis (3) is reduced during aging in vivo.…”