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Related Experiment Videos

Receptors bound to antiprogestin from abortive complexes with hormone responsive elements.

A Guiochon-Mantel1, H Loosfelt, T Ragot

  • 1Hormones et Reproduction (INSERM U135), Faculté de Médecine, Paris-Sud, Le Kremlin Bicêtre, France.

Nature
|December 15, 1988
PubMed
Summary

Antisteroids inhibit hormone action by blocking receptor binding to DNA. This study shows antiprogestin RU486 blocks constitutive receptor activity, revealing inhibition occurs at the DNA-responsive element level.

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Area of Science:

  • Molecular Endocrinology
  • Steroid Hormone Action
  • Gene Regulation

Background:

  • The precise mechanism by which antisteroids exert their effects remains unclear.
  • Proposed mechanisms include trapping receptors in non-DNA-binding states or inducing non-specific DNA binding.
  • Antisteroid-receptor complexes may also bind hormone-responsive elements (HREs) but form non-functional transcriptional complexes.

Purpose of the Study:

  • To investigate the mechanism of antisteroid action by bypassing early steps of hormone receptor regulation.
  • To determine if antisteroids inhibit constitutive receptor activity.

Main Methods:

  • Constructed a deleted cDNA for a constitutively active mutant rabbit progesterone receptor.
  • Utilized co-transfection experiments to express both constitutive and wild-type receptors in the same cells.

Related Experiment Videos

  • Assessed the effect of antiprogestin RU486 on reporter gene activity driven by these receptors.

    • Main Results:

    • The constitutively active receptor bound to HREs independently of hormone.
    • Antiprogestin RU486-wild-type receptor complexes effectively suppressed the activity of the constitutive receptor.
    • This suppression occurred even when both receptors shared the same HREs.

    Conclusions:

    • Antisteroid inhibition of progesterone receptor activity occurs at the level of the hormone-responsive element.
    • The study provides evidence that antisteroids can interfere with receptor binding or function at the DNA level.
    • This mechanism bypasses the need for hormone-induced receptor activation or initial DNA binding steps.