Messenger RNA Stabilization and Gene Transcription in the Estrogen Induction of Vitellogenin mRNA

Shapiro, David J.; Brock, Martin L.

doi:10.1016/b978-0-12-452812-3.50009-9

Cited by 23 publications

(11 citation statements)

References 84 publications

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“…Furthermore, ERE having stimulatory effects on transcriptional activity may be responsible for regulation of the PR gene. Estradiol may also influence the half-life of preexisting mRNA species, represented by selective stabilization or degradation of specific mRNAs in the absence or presence of the hormone (28). The mechanisms for such interactions are, however, poorly defined.…”

Section: Discussionmentioning

confidence: 97%

Autologous Down-Regulation of Messenger Ribonucleic Acid and Protein Levels for Estrogen Receptors in MCF-7 Cells: An Inverse Correlation to Progesterone Receptor Levels*

Ree

Landmark²,

Eskild³

et al. 1989

Endocrinology

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In the present study we have examined the effects of estradiol on mRNA levels for estrogen (ER) and progesterone receptors (PR) in the estrogen-dependent mammary carcinoma MCF-7 cell line. The changes in ER immunoactivity and specific binding of [3H]R5020 were also assessed. Estradiol (10(-7) M) caused a transient and time-dependent reduction of the level of mRNA for ER, with a maximal effect (30-40% of control; n = 3) after 72 h. This was associated with a similar decrease in ER immunoactivity. Further treatment (96 and 120 h) revealed a return of ER mRNA to control values, whereas the ER immunoactivity remained depressed. The effect on the mRNA level for PR gave almost the inverse curve. Initially (24-72 h), we observed a pronounced increase in this mRNA, with a maximal effect (6-7 times the control value; n = 3) after 72 h. Treatment beyond 72 h was associated with a gradual return of mRNA for PR toward the control level. The variation in specific binding of [3H]R5020 revealed similar changes, except that changes in specific receptor binding were delayed 24 h compared to the levels of mRNA. Incubation with low concentrations (10(-11) and 10(-10) M) of estradiol for 72 h was associated with slightly elevated levels of mRNA for ER, whereas higher concentrations gave a dose-dependent decrease. The mRNA for PR was biphasically stimulated, with a maximal effect at 10(-10)-10(-8) M, where a 10- to 13-fold stimulation was observed. The highest concentration (10(-7) M) gave a lower response. Assessment of concentration-induced variations in protein receptor levels of ER and PR reflected the effects of estradiol on their mRNAs. Low concentrations of estradiol slightly enhanced the ER level, whereas high concentrations clearly reduced ER immunoactivity. The PR level was stimulated by all concentrations used, and 10(-8) M estradiol raised the PR level more than 11-fold. Our results indicate autologous regulation of estrogen receptor gene transcripts and proteins and a clear induction of PR mRNA and receptor proteins by estradiol.

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Section: Discussionmentioning

confidence: 97%

Autologous Down-Regulation of Messenger Ribonucleic Acid and Protein Levels for Estrogen Receptors in MCF-7 Cells: An Inverse Correlation to Progesterone Receptor Levels*

Ree

Landmark²,

Eskild³

et al. 1989

Endocrinology

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“…Therefore different mRNAs can be differentially regulated within the same cell type at the level of turnover. Precedent for cell-specific changes in the stability of a given mRNA lies in the many instances where the stability of a specific mRNA is affected by a developmental or a regulatory signal (56)(57)(58)(59)(60).…”

Section: Discussionmentioning

confidence: 99%

Tissue-specific genetic variation in the level of mouse alcohol dehydrogenase is controlled transcriptionally in kidney and posttranscriptionally in liver.

Tussey

Felder²

1989

Proc. Natl. Acad. Sci. U.S.A.

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Tissue-specific genetic variation in expression of the alcohol dehydrogenase, encoded by the Adh-i gene, is found between C57BL/6J (B6) mice and B6.S congenic mice. B6.S mice contain a variant Adh-1 allele derived from a wild Danish strain in a B6 genetic background. B6 mice have nearly twice the alcohol dehydrogenase activity in liver but less than half the activity in kidney as B6.S mice. These tissue-specific genetic changes in alcohol dehydrogenase expression are manifest at the level of Adh-i-encoded mRNA. The regulatory site(s) involved act cis in both kidney and liver. These strains also differ in the extent to which androgen induces mRNA encoded by kidney Adh-1, with androgen increasing these levels 17-fold and 7.4-fold in the B6 and B6.S kidney, respectively. To identify the regulatory mechanism(s) underlying this strain variation in Adh-l expression, estimates were obtained for the relative rate ofAdh-1 transcription in the B6 and B6.S kidney, liver, and androgen-induced kidney. For both uninduced and induced kidney, a difference in the transcription rate alone accounts for the strain difference in mRNA concentration. In contrast, because the Adh-l transcription rate in liver does not differ significantly between B6 and B6.S mice, strain-specific variation in posttranrscriptional regulation must be operative.Taken together these results indicate that the variation in Adh-1 expression between B6 and B6.S mice results from changes in both transcriptional and posttranscriptional control, and these controls are differentially operative in kidney and liver.

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“…Several mechanisms for the steroid-mediated induction of mRNAs have been described, including transcriptional activation, mRNA stabilization, and a combination of the two (1,26). The most intensively studied systems have tended to be responses to glucocorticoids or estrogens.…”

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confidence: 99%

mRNA synthesis rates in vivo for androgen-inducible sequences in mouse kidney.

Watson¹,

Paigen²

1988

Mol. Cell. Biol.

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A method was developed for measuring in vivo rates of mRNA synthesis in mice by pulse-labeling with the RNA precursor [3Hlorotate and then using hybridization to recover specific mRNAs. The efficiency of recovery is determined with synthetic RNAs as internal hybridization standards. The method is particularly applicable to the kidney since this organ shows a strong preferential uptake of the label. Rates of synthesis, expressed as a fraction of total RNA synthesis, were measured for the androgen-inducible mRNAs coding for Iglucuronidase (GUS), ornithine decarboxylase (ODC), the protein coded by the RP-2 gene, and the so-called kidney androgen-regulated protein (KAP). Control mRNAs coded for 1-actin, phosphoenolpyruvate carboxykinase, and major urinary protein. Testosterone markedly increased the synthesis of the androgen-inducible mRNAs, but not the control mRNAs. Induction was not seen in mutant mice lacking functional androgen receptor protein. For GUS, ODC, and RP-2 mRNAs, the fold induction of synthesis was less than the fold induction of concentration, suggesting that mRNA stabilization also plays a part in the response to androgen. For GUS, ODC, and RP-2 mRNAs, but not KAP mRNA, induction of synthesis was rapidly reversed after testosterone removal. KAP mRNA was also exceptional in that its concentration was disproportionately high compared with its rate of synthesis, implying that it is a particularly stable mRNA.Several mechanisms for the steroid-mediated induction of mRNAs have been described, including transcriptional activation, mRNA stabilization, and a combination of the two (1, 26). The most intensively studied systems have tended to be responses to glucocorticoids or estrogens. Less is known about the mechanisms of response to androgenic steroids, which have been shown to produce a variety of secondary sex responses in several different tissues (3). In mouse kidney, several specific mRNAs are induced by androgens and these vary from each other in both the time course and the extent of induction (5-7, 29, 32, 33). A major question is whether or not these inductions are at the level of mRNA synthesis.In previous studies, transcription rates of mRNAs for ornithine decarboxylase (ODC), kidney androgen-regulated protein (KAP), and the RP-2 gene product were measured by the nuclear runoff method both before and after induction by androgen (6). No significant changes in transcription rates were detected, and it was concluded that androgen regulation of these three sequences is posttranscriptional. Because the kinetics of deinduction after removal of hormone were substantially faster than the kinetics of induction for both ODC and RP-2 mRNAs, it was suggested that androgen effects a stabilization of these mRNAs (6). The kinetics of induction and deinduction were also studied for 3-glucuronidase (GUS) mRNA, which is another androgen-responsive mRNA in mouse kidney. Again, induction was significantly slower than deinduction; however, in this case the difference was not sufficient to account for the full ext...

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Messenger RNA Stabilization and Gene Transcription in the Estrogen Induction of Vitellogenin mRNA

Cited by 23 publications

References 84 publications

Autologous Down-Regulation of Messenger Ribonucleic Acid and Protein Levels for Estrogen Receptors in MCF-7 Cells: An Inverse Correlation to Progesterone Receptor Levels*

Autologous Down-Regulation of Messenger Ribonucleic Acid and Protein Levels for Estrogen Receptors in MCF-7 Cells: An Inverse Correlation to Progesterone Receptor Levels*

Tissue-specific genetic variation in the level of mouse alcohol dehydrogenase is controlled transcriptionally in kidney and posttranscriptionally in liver.

mRNA synthesis rates in vivo for androgen-inducible sequences in mouse kidney.

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