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Transactivation functions facilitate the disruption of chromatin structure by estrogen receptor derivatives in vivo

T A Pham1, Y P Hwung, D P McDonnell

  • 1Department of Cell Biology, Baylor College of Medicine, Houston, Texas 77030.

The Journal of Biological Chemistry
|September 25, 1991
PubMed

Insights

Estrogen receptor binding and transactivation enhance chromatin structure alterations at gene promoters. This disruption creates a nucleosome-free window essential for initiating transcription in vivo.

Area of Science:

  • Molecular Biology
  • Genetics
  • Biochemistry

Background:

  • Nuclear receptors activate gene transcription through chromatin structure modifications.
  • Estrogen receptor (ER) binding to DNA alters chromatin at target genes.
  • Understanding these molecular mechanisms is crucial for gene regulation studies.

Purpose of the Study:

  • To investigate the role of DNA binding and transactivation by ER derivatives.
  • To analyze ER-mediated chromatin structure changes at estrogen-responsive reporter minichromosomes.
  • To elucidate the molecular functions underlying receptor-mediated chromatin alterations.

Main Methods:

  • Utilized Saccharomyces cerevisiae as a model system.
  • Employed reporter minichromosomes with estrogen-responsive elements.
  • Evaluated DNase I-hypersensitive chromatin structure in response to ER derivatives.

Main Results:

  • Promoter chromatin structure alterations are enhanced by ER transactivation functions, not just DNA binding.
  • These chromatin changes depend on multiple estrogen-responsive elements and downstream promoter sequences.
  • Chromatin alterations correlate with promoter transcriptional competence.

Conclusions:

  • Receptor-mediated disruption of chromatin structure is linked to active transcription complex formation.
  • This local chromatin disruption likely creates a nucleosome-free window for transcription initiation.
  • Findings suggest a mechanism for how nuclear receptors establish transcriptional competence.

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