Stimulation of RNA polymerase I and II activities by 17β-estradiol receptor on chick liver chromatin

Abstract

The endogenous transcriptional capacity (RNA polymerase I and II activity) of liver chromatin from chicks treated with 17 beta-estradiol for 24 h (E 24) was double that of the controls. E 24 chromatin contained estradiol receptor activity while control chromatin did not. Its presence suggested an implication in the enhanced activities of RNA polymerases of E 24 chromatin. When semi-purified estradiol receptor was added to control chromatin, the endogenous transcriptional capacity of this chromatin was greatly increased. Studies with alpha-amanitin showed that both RNA polymerase I and II were stimulated by the estradiol receptor. This stimulation was observed as long as homology of the system was maintained. Solubilized homologous RNA polymerases were stimulated much less by the hormone complex in the presence of heterologous DNA than with homologous chromatin. Prokaryotic RNA polymerase could not be stimulated by chick liver estradiol receptor in the presence of heterologous DNA.

Pharmacologic activation of estrogen receptor α increases mitochondrial function, energy expenditure, and brown adipose tissue

“…The pharmacologic functions of estrogens are mediated principally by estrogen receptors (ERs) a and b as well as by a membrane receptor (26–28). In vitro and in vivo models provide evidence for the involvement of these receptors in obesity and cholesterol metabolism (29–31).…”

Vitellogenin synthesis in isolated hepatocytes

“…Whether for this reason the hepatocytes failed to synthesize vitellogenin, we do not know at the moment. In vivo, the increased RNA polymerase activities are mediated through the estradiol receptor complex as we have shown in reconstitution experiments [18,19].…”