Negative regulation of chicken GATA-1 promoter activity mediated by a hormone response element

Mol Endocrinol. 1995 Sep;9(9):1135-46. doi: 10.1210/mend.9.9.7491106.

Abstract

GATA-1 is a DNA-binding protein that regulates transcription of erythroid-specific genes and is required for the formation of mature erythroid cells. We show here that the GATA-1 hormone response-like element (GHRE) within the first intron of the gene functions as an inhibitory element in chicken erythroid precursor cells, as revealed by expression studies with mutants of the minimal GATA-1 promoter. We identify in these precursor cells the relevant proteins that interact with GHRE as a heterodimer of the thyroid hormone receptor alpha and the chicken ovalbumin upstream promoter transcription factor. Our results indicate that this novel complex can negatively regulate the GATA-1 promoter and suggest that GATA-1 can overcome this inhibitory action. We provide evidence that the viral gene product, v-erb A, can also reduce GATA-1 promoter activity through the GHRE site.

MeSH terms

  • Animals
  • Base Sequence
  • Binding Sites
  • Binding, Competitive
  • COUP Transcription Factor I
  • Chickens / genetics
  • DNA / chemistry
  • DNA / metabolism
  • DNA-Binding Proteins / genetics*
  • DNA-Binding Proteins / immunology
  • DNA-Binding Proteins / physiology
  • Erythroid Precursor Cells / metabolism
  • Erythroid-Specific DNA-Binding Factors
  • Gene Expression Regulation*
  • Hormones / pharmacology*
  • Introns
  • Molecular Sequence Data
  • Mutagenesis
  • Promoter Regions, Genetic*
  • Receptors, Thyroid Hormone / immunology
  • Receptors, Thyroid Hormone / physiology
  • Regulatory Sequences, Nucleic Acid*
  • Transcription Factors / genetics*
  • Transcription Factors / immunology
  • Transcription Factors / physiology
  • Transfection
  • Triiodothyronine / pharmacology

Substances

  • COUP Transcription Factor I
  • DNA-Binding Proteins
  • Erythroid-Specific DNA-Binding Factors
  • Hormones
  • Receptors, Thyroid Hormone
  • Transcription Factors
  • Triiodothyronine
  • DNA