Induction of estrogen receptor and reversal of the nuclear/cytoplasmic receptor ratio during vitellogenin synthesis and withdrawal in Xenopus laevis

• Published in: The Journal of biological chemistry 1980-12, Vol.255 (23), p.11308-11312
• Main Authors: Hayward, M A, Mitchell, T A, Shapiro, D J
• Format: Article
• Language: English
• Subjects: Animals; Binding, Competitive; Cell Nucleus - metabolism; Cytosol - metabolism; Estradiol - metabolism; Estradiol - pharmacology; Kinetics; Lipoproteins - biosynthesis; Liver - drug effects; Liver - metabolism; Male; Receptors, Estrogen - drug effects; Receptors, Estrogen - metabolism; RNA, Messenger - metabolism; Vitellogenins - biosynthesis; Xenopus
• ISSN: 0021-9258; 1083-351X
• DOI: 10.1016/s0021-9258(19)70292-0

The levels of cytoplasmic and nuclear estrogen receptor have been determined in livers of male Xenopus laevis stimulated by estradiol-17 beta to synthesize vitellogenin mRNA. Estrogen receptor levels were also determined in unstimulated liver and following long term withdrawal of estrogen. In unstimulated liver cells, which do not contain detectable vitellogenin mRNA, more than 80% of the estrogen receptor is located in the nucleus (550 high affinity estrogen binding sites/nucleus), while the cytoplasm contains only 100 high affinity estrogen binding sites/cell. Administration of estradiol-17 beta, which induces massive synthesis and accumulation of vitellogenin mRNA, induces the estrogen receptor as well. The nuclear receptor level rises to approximately 2,000 estrogen binding sites/cell, while the cytosol receptor increases to only 150 sites/cel. Liver cells of male X. laevis which have been withdrawn from estrogen for 70 days exhibit a striking change in receptor levels. The nuclear receptor returns to the level prevailing in unstimulated cells (approximately 500 sites/cell) while the cytosol receptor level rises to more than 1,200 sites/cell (equivalent to 260 fmol/g of tissue). The existence of a pool of cytosol receptor, which is rapidly available for induction of vitellogenin mRNA, may in part explain the shorter lag period and more rapid induction of vitellogenin mRNA observed during secondary estrogen stimulation of withdrawn Xenopus liver cells.