Regulation of Egr-1-dependent gene expression by the C-terminal activation domain

Biochem Biophys Res Commun. 1999 Feb 16;255(2):208-15. doi: 10.1006/bbrc.1999.0182.

Abstract

The present study analyzes the role of the C-terminal activation domain for Egr-1 transcriptional activity using N-terminal deletion mutants. Mutant N372 comprising the entire C-terminal activation domain and partly truncated DNA-binding and nuclear translocation domains functioned as the transdominant repressor of Egr-1-dependent gene transcription. Activity of the SV40 promoter, however, was not affected by the N372 mutant. Analysis of additional Egr-1 mutants revealed that the transdominant negative effect of N372 was dependent on truncation of the zinc finger motifs that mediate DNA binding. Reconstitution of the zinc fingers was sufficient to generate Egr-1 proteins with potent transcriptional activity. The inhibitory mutant N372 is efficiently translocated to the nucleus, but fails to bind DNA and does not displace DNA-bound wildtype Egr-1. These results provide evidence for an Egr-1-specific cofactor that interacts with the C-terminal activation domain and is essential for Egr-1 transcriptional activity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3T3 Cells
  • Animals
  • Binding Sites / genetics
  • Cell Line
  • Consensus Sequence
  • DNA / metabolism
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / physiology*
  • Early Growth Response Protein 1
  • Gene Expression Regulation*
  • Genes, Dominant
  • Humans
  • Immediate-Early Proteins*
  • Kidney / cytology
  • Mice
  • Mutagenesis, Insertional
  • Peptide Fragments / genetics
  • Peptide Fragments / physiology*
  • Protein Binding / genetics
  • Protein Structure, Tertiary
  • Transcription Factors / genetics
  • Transcription Factors / physiology*
  • Transcription, Genetic

Substances

  • DNA-Binding Proteins
  • EGR1 protein, human
  • Early Growth Response Protein 1
  • Egr1 protein, mouse
  • Immediate-Early Proteins
  • Peptide Fragments
  • Transcription Factors
  • DNA