c-Myb and members of the c-Ets family of transcription factors act as molecular switches to mediate opposite steroid regulation of the human glucocorticoid receptor 1A promoter

J Biol Chem. 2005 Dec 30;280(52):43264-71. doi: 10.1074/jbc.M508245200. Epub 2005 Nov 1.

Abstract

Steroid auto-regulation of the human glucocorticoid receptor (hGR) 1A promoter in lymphoblast cells resides largely in two DNA elements (footprints 11 and 12). We show here that c-Myb and c-Ets family members (Ets-1/2, PU.1, and Spi-B) control hGR 1A promoter regulation in T- and B-lymphoblast cells. Two T-lymphoblast lines, CEM-C7 and Jurkat, contain high levels of c-Myb and low levels of PU.1, whereas the opposite is true in IM-9 B-lymphoblasts. In Jurkat cells, overexpression of c-Ets-1, c-Ets-2, or PU.1 effectively represses dexamethasone-mediated up-regulation of an hGR 1A promoter-luciferase reporter gene, as do dominant negative c-Myb (c-Myb DNA-binding domain) or Ets proteins (Ets-2 DNA-binding domain). Overexpression of c-Myb in IM-9 cells confers hormone-dependent up-regulation to the hGR 1A promoter reporter gene. Chromatin immunoprecipitation assays show that hormone treatment causes the recruitment of hGR and c-Myb to the hGR 1A promoter in CEM-C7 cells, whereas hGR and PU.1 are recruited to this promoter in IM-9 cells. These observations suggest that the specific transcription factor that binds to footprint 12, when hGR binds to the adjacent footprint 11, determines the direction of hGR 1A promoter auto-regulation. This leads to a "molecular switch" model for auto-regulation of the hGR 1A promoter.

MeSH terms

  • Apoptosis
  • B-Lymphocytes / metabolism*
  • Blotting, Western
  • Cell Line
  • Cell Lineage
  • Chromatin Immunoprecipitation
  • DNA-Binding Proteins / biosynthesis*
  • Electroporation
  • Exons
  • Gene Expression Regulation*
  • Genes, Dominant
  • Humans
  • Jurkat Cells
  • Leukemia / metabolism
  • Luciferases / metabolism
  • Lymphocytes / metabolism
  • Models, Biological
  • Polymerase Chain Reaction
  • Promoter Regions, Genetic*
  • Protein Binding
  • Protein Structure, Tertiary
  • Proto-Oncogene Protein c-ets-1 / biosynthesis*
  • Proto-Oncogene Protein c-ets-2 / biosynthesis*
  • Proto-Oncogene Proteins / biosynthesis*
  • Proto-Oncogene Proteins / metabolism
  • Proto-Oncogene Proteins c-ets / metabolism
  • Proto-Oncogene Proteins c-ets / physiology*
  • Proto-Oncogene Proteins c-myb / metabolism
  • Proto-Oncogene Proteins c-myb / physiology*
  • Receptors, Glucocorticoid / genetics*
  • Steroids / metabolism*
  • T-Lymphocytes / cytology
  • T-Lymphocytes / metabolism*
  • Trans-Activators / biosynthesis*
  • Trans-Activators / metabolism
  • Transcription Factors / biosynthesis*
  • Transfection
  • Up-Regulation

Substances

  • DNA-Binding Proteins
  • ETS1 protein, human
  • Proto-Oncogene Protein c-ets-1
  • Proto-Oncogene Protein c-ets-2
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-ets
  • Proto-Oncogene Proteins c-myb
  • Receptors, Glucocorticoid
  • Steroids
  • Trans-Activators
  • Transcription Factors
  • proto-oncogene protein Spi-1
  • SPIB protein, human
  • Luciferases