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Mutations of the rat growth hormone promoter which increase and decrease response to thyroid hormone define a

G A Brent1, J W Harney, Y Chen

  • 1Department of Molecular Biology, Massachusetts General Hospital, Boston 02114.

Molecular Endocrinology (Baltimore, Md.)
|December 1, 1989
PubMed
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Thyroid hormone (T3) response elements in the rat growth hormone promoter were studied using mutations. Perfecting repeat sequences significantly boosted T3 induction, highlighting the importance of specific DNA sequences for gene regulation.

Area of Science:

  • Molecular Biology
  • Genetics
  • Endocrinology

Background:

  • Thyroid hormone (T3) regulates gene expression, including the rat growth hormone (rGH) gene.
  • Specific DNA sequences upstream of the rGH gene promoter are known to mediate T3 induction.

Purpose of the Study:

  • To identify and characterize the functional significance of specific DNA domains within the T3-responsive region of the rGH promoter.
  • To elucidate the role of direct repeats and inverted copies in mediating T3-induced gene expression.

Main Methods:

  • Site-directed mutagenesis of synthetic DNA sequences corresponding to domains A, B, and C within the rGH promoter region.
  • Functional analysis of mutant promoter constructs in reporter gene assays (T3 induction).
  • In vitro binding assays to assess receptor-DNA interactions.

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Main Results:

  • Mutations enhancing the similarity of domain B to domain A significantly increased T3 induction.
  • A point mutation in domain C improving its match to domain A also boosted T3 induction.
  • All three domains (A, B, C) were found to contribute to the amplified T3 response, with binding affinity correlating with functional response.

Conclusions:

  • The study proposes a consensus T3 receptor binding half-site (AGGT(C/A)A).
  • At least two copies of this half-site are required for a functional T3 response.
  • Specific DNA sequence arrangements, including imperfect repeats, are crucial for amplified T3-mediated gene regulation.