Long-term effects of estrogen on avian liver: estrogen-inducible switch in expression of nuclear, hormone-binding proteins.

Abstract

The stimulation of chicks or embryos with estrogen results in transient, hepatic expression of the vitellogenin gene, as well as long-term, propagatable alterations in the rapidity with which the gene can be reactivated. We examined the possibility that nuclear, type H estrogen-binding sites are involved in this long-term change in response characteristics. We demonstrate that the primary induction kinetics of type II sites in embryos and chicks correlated with the expression of the vitellogenin gene and that once their induction was triggered by estrogen, they accumulated, were propagated, and persisted for months after withdrawal of the hormone. We also show that their accumulation in the embryo was accompanied by prolonged expression of both the vitellogenin and very low-density apolipoprotein II genes, in the absence of elevated levels of type I receptor, and that the type II sites, like the classical receptor, appear to be preferentially associated with active or potentially active chromatin. Finally, we describe a regulatory mechanism, tested by computer modelling, that simulated the behavioral characteristics of these nuclear estrogen-binding sites and which may explain their role in mediating the long-term effects of estrogen.

Transient administration of estradiol-17 beta establishes an autoregulatory loop permanently inducing estrogen receptor mRNA.

“…In a series of studies, Deeley and coworkers have established that estrogen elicits a long-term induction of apolipoproteins in cultured human cells and in avian liver (16,17). In contrast to Xenopus liver, they find that the avian liver high-affinity type I nuclear estrogen receptor is only transiently induced by estrogen (17).…”

“…In a series of studies, Deeley and coworkers have established that estrogen elicits a long-term induction of apolipoproteins in cultured human cells and in avian liver (16,17). In contrast to Xenopus liver, they find that the avian liver high-affinity type I nuclear estrogen receptor is only transiently induced by estrogen (17). Since they observe the long-term estrogen induction of a lower affinity type II estrogen-binding protein, they propose that this protein mediates the persistent effects of estrogen by serving as a constitutive estrogen-independent activator of gene transcription (17).…”

Developmental regulation of specific protein interactions with an enhancerlike binding site far upstream from the avian very-low-density apolipoprotein II gene.

“…The competence to express the apoVLDLII gene and other members of this group, such as the vitellogenin genes, as well as the extent to which they respond, has been correlated with increases in the hormone-dependent inducibility of the hepatic estrogen receptor (16,17). Induction of the receptor is first detectable at approximately days 9 to 10 of embryogenesis (16,17,21). The extent to which it can be induced then increases markedly during later stages of development.…”

Effects of ovariectomy and estrogen replacement on attractivity and receptivity in the red-sided garter snake (Thamnophis sirtalis parietalis)

“…This restriction does not appear to be necessary in female snakes unless the low level of estrogen remaining in ovariectomized animals is sufficient to induce genomic, long-term changes. An alternative mechanism may be that of "gene memory", where estrogen can exert long-term effects on the genome that persist in the absence of the steroid and then elicit a more rapid response when the stimulus is re-instated (Burch and Evans 1986;Hache et al 1987;Crews 1991;Pfaff et al 1994).…”