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Related Experiment Videos

Progestin receptors: isoforms and antihormone action.

H Gronemeyer1, M E Meyer, M T Bocquel

  • 1Laboratoire de Génétique Moléculaire des Eucaryotes du CNRS, Institut de Chimie Biologique, Faculté de Médecine, Strasbourg, France.

The Journal of Steroid Biochemistry and Molecular Biology
|January 1, 1991
PubMed
Summary

The chicken and human progesterone receptors (PR) isoforms A and B arise from distinct mRNA populations, regulated by unique promoters. Estrogen influences hPR gene expression, and both PR isoforms activate transcription differently.

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Area of Science:

  • Molecular Biology
  • Endocrinology
  • Genetics

Background:

  • The progesterone receptor (PR) is a key regulator of reproductive processes.
  • PR exists in two main isoforms, A and B, with distinct functions.
  • Understanding the regulation of PR isoforms is crucial for reproductive health and disease.

Purpose of the Study:

  • To investigate the origins of chicken (cPR) and human (hPR) progesterone receptor isoforms A and B.
  • To identify the regulatory elements controlling the expression of different PR transcripts.
  • To elucidate the transcriptional activation mechanisms of PR isoforms and the action of anti-progestins.

Main Methods:

  • mRNA population analysis
  • Promoter identification and characterization

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  • Transcriptional activation assays
  • Analysis of anti-progestin RU486 mechanism

    • Main Results:

    • Two distinct mRNA populations generate cPR and hPR isoforms A and B.
    • Alternative translation initiation sites produce isoform A from a downstream AUG.
    • Two estrogen-inducible hPR promoters identified; cPR promoter suggests cell-type specific auto-regulation.
    • Estrogen induction of cPR expression occurs post-transcriptionally.
    • hPR isoforms A and B exhibit promoter-specific transcriptional activation.

    Conclusions:

    • PR isoforms A and B originate from separate mRNA populations regulated by distinct promoters.
    • Estrogen modulates hPR gene expression through specific promoters.
    • Cell-type and isoform-specific auto-regulation of cPR transcription is suggested.
    • Estrogen induction of cPR is post-transcriptional.
    • PR isoforms differentially activate transcription, with implications for anti-progestin action.