The role of estrogen receptor in Xenopus laevis vitellogenin gene expression

Abstract

Administration of estradiol 17 beta [estra-1,3,5(10)-triene-3,17-beta-diol] to male Xenopus laevis induces the massive synthesis by the liver of the egg yolk precursor phospholipoglycoprotein, vitellogenin, and its cognate mRNAs. Restimulation of male X. laevis that have been previously induced to synthesize vitellogenin mRNA but are inactive in vitellogenin mRNA synthesis at the time of restimulation with estrogen results in more rapid accumulation of vitellogenin mRNA and more efficient transcription of the vitellogenin genes than occurs following primary estrogen stimulation. The estrogen receptor system that mediates estrogen action in this organism exhibits several unusual properties. The cytoplasm of unstimulated liver cells contains high levels of a middle-affinity estrogen-specific binding protein and little if any estrogen receptor. The properties of the estrogen binding protein are consistent with a role in protecting estradiol 17 beta against metabolism, as a fraction of cytoplasmic estradiol 17 beta is not subject to rapid metabolism. In addition, similar binding activities are found in all Xenopus tissues surveyed that respond to steroid hormones. The induction of nuclear estrogen receptor is coincident with the onset of vitellogenin mRNA accumulation. However, an increased level of estrogen receptor is not responsible for the elevated rate of vitellogenin gene transcription observed following restimulation with estrogen.

In vivo estrogen induction of hepatic estrogen receptor mRNA and correlation with vitellogenin mRNA in rainbow trout

“…However, while the level of rtER mRNA is not maintained and returns to the basal value 3 weeks after primary injection, we still observed a memory effect on the induction of Vg gene following the second injection. To explain this memory effect, we cannot invoke the presence of a higher level of receptors at the time of the second injection as in Xenopus or chicken liver (Westley and Knowland, 1979;Hayward et al, 1982;Tata et al, 1987). Persistent structure modification of the Vg gene, or the presence of additional transcription factors, is more likely to explain the phenomenon.…”

“…This memory effect persists for as long as 6 months and is passively maintained through cell division (Burch and Evans, 1986). Different hypotheses have been proposed to explain this phenomenon, for example either the maintaining of a high level of estrogen receptors (Westley and Knowland, 1979;Tata et al, 1987) or the presence of an estrogen-binding protein (Hayward et al, 1982), but persistent modification of the structure of the vitellogenin gene has also been suggested (Tata and Baker, 1975;Gerber et al, 1981;Burch and Weintraub, 1983). We have previously described the cloning, sequencing and in vitro expression of a full-length random trout estrogen receptor cDNA (rtER cDNA) (Pakdel et al, 1990).…”

Sex Differences: A Resultant of an Evolutionary Pressure?

“…In higher phyla estrogens and their receptors (ER) acquired an indispensable role in the reproductive organs, where controlled the mechanisms leading to the maturation of the egg, and in the liver, where became essential for vitellogenin synthesis (Della Torre et al, 2014;Flouriot et al, 1997;Flouriot et al, 1996;Hayward et al, 1982;May et al, 1981;Nagler et al, 2000;Pakdel et al, 1991;Takase and Iguchi, 2007). Supporting this view, from anguilliformes to mammals, ER expression or activity is highest in ovaries and liver (Ciana et al, 2003;Griffin et al, 1999;Nagler et al, 2000;Todo et al, 1996).…”

RNA-Seq-based transcriptome analysis of Korean rose bitterling (Rhodeus uyekii) exposed to synthetic estrogen 17-α-ethinylestradiol (EE2)

“…The induction of the estrogen receptor (ER) is coincident with the onset of vitellogenin mRNA accumulation (Hayward et al, 1982). Annotation data showed that treatment with 100 ng/L EE2 affected the transcription of vitellogenin (comp64337_c0_seq1), ER comp103131_c0_seq17) and anti-Mullerian hormone (comp88901_c0_seq4).…”