Steroid Hormones Differentially Induce Transcription of the Chicken Ovalbumin Gene, but Stabilize the mRNA with the Same Half-Life

Abstract

The stabilization of chicken ovalbumin (OVA) mRNA by different classes of steroid hormones (estrogen, progesterone, glucocorticoid, and androgen) was studied in the oviducts of chicks treated with combinations of four steroids. The combination of estrogen with progesterone, glucocorticoid, or androgen enhanced the induction of the OVA gene more than did estrogen alone. Run-on analysis of the isolated oviduct nuclei to measure the transcription rate of the OVA gene showed that the enhanced induction of the OVA gene by the combined hormone treatments was partly caused by an increased rate of transcription. The half-life of OVA mRNA as determined using a transcription inhibitor (actinomycin D) was estimated to be about 24 h irrespective of the hormone treatment, though the half-life was about 6 h in the absence of hormones. These results suggested that the prolongation of the half-life of OVA mRNA by steroid hormones is constant irrespective of differential transcription rates of the OVA gene.

Gonadotropin-induced changes in oviducal mRNA expression levels of sex steroid hormone receptors and activin-related signaling factors in the alligator

“…In leopard gecko, shell gland differentiation positively correlates with circulating androgen level, whereas AR mRNA expression negatively correlates with the degree of shell gland differentiation [53]. In chicken oviducts, estrogen and progesterone induce the transcription of ovoalbumin; co-treatment with androgens enhance this induction [1]. These results support a role for androgen signaling in oviducal regulation across tetrapods.…”

Upstream Stimulatory Factor (USF) Is Recruited into a Steroid Hormone-triggered Regulatory Circuit by the Estrogen-inducible Transcription Factor δEF1

“…This is due to a 20-fold increase of transcription of the Ov gene (7) coupled with a 10-fold increase in mRNA stability (8). The Ov gene is classified as a secondary response gene because the estrogen receptor does not directly bind to it and because there is a requirement for concomitant protein synthesis for transcriptional activation (9).…”