ELF-1 interacts with and transactivates the IgH enhancer pi site

J Biol Chem. 1996 Oct 18;271(42):26007-12. doi: 10.1074/jbc.271.42.26007.

Abstract

We previously identified a B-cell-specific regulatory element in the immunoglobulin heavy chain (IgH) enhancer, pi, with striking similarity to binding sites for ets-related transcription factors. Whereas the ability of ets-related factors to bind to and transactivate the pi site has been substantiated, the identification of the particular member of the ets family responsible for B-cell-specific regulation of the pi site has remained controversial. We have used antibodies specific for individual members of the ets family to evaluate which ets-related factor in B-cell nuclear extracts interacts with the IgH pi site. We present strong evidence that ELF-1 is highly expressed in B-cells and is one of two major factors specifically interacting with the murine IgH enhancer pi site in B-cell nuclear extracts. Binding of ELF-1 correlates with activity of the pi site, since mutations abolishing function of pi also inhibit binding of ELF-1. Furthermore, we demonstrate that ELF-1 can transactivate the IgH enhancer in HeLa cells, suggesting a role for ELF-1 in B-cell-specific IgH gene expression.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • B-Lymphocytes / metabolism
  • Base Sequence
  • Cells, Cultured
  • Consensus Sequence
  • DNA-Binding Proteins / metabolism*
  • Enhancer Elements, Genetic*
  • HeLa Cells
  • Immunoglobulin Heavy Chains / genetics*
  • Mice
  • Molecular Sequence Data
  • Mutagenesis, Site-Directed
  • Nuclear Proteins
  • Transcription Factors / metabolism*
  • Transcriptional Activation*

Substances

  • DNA-Binding Proteins
  • ELF1 protein, human
  • Elf1 protein, mouse
  • Immunoglobulin Heavy Chains
  • Nuclear Proteins
  • Transcription Factors