The non‐histone chromosomal protein HMG‐I(Y) contributes to repression of the immunoglobulin heavy chain germ‐line ε RNA promoter

Jinny Kim, Ray Reeves, Paul Rothman, Mark Boothby

Research output: Contribution to journalArticlepeer-review

Abstract

The rate of germ‐line RNA transcription correlates with the rate of immunoglobulin heavy chain isotype switching. A promoter element for the transcription of RNA from the germ‐line mouse immunoglobulin ε heavy chain constant region gene is induced by interleukin(IL)‐4 and lipopolysaccharide, and is bound at its transcription initiation sites by an IL‐4‐inducible nuclear protein, NF‐BRE. To examine the function of the binding site for this IL‐4‐inducible complex, substitution mutations were introduced in the promoter. These binding site mutations increased promoter activity and decreased binding of NF‐BRE. To investigate the paradox of an IL‐4‐inducible protein binding to a repressor site in an IL‐4‐inducible promoter, we determined that the non‐histone chromosomal protein HMG‐I(Y) binds at the transcription initiation sites of the germ‐line epsilon promoter. Assays with antisera against HMG‐I(Y) revealed monomeric HMG‐I(Y) in nuclear extracts. Cotransfection of an expression construct directing the synthesis of anti‐sense HMG‐I(Y) RNA also increased promoter activity, consistent with a repressor function of HMG‐I(Y). Thus, the data are most consistent with a model in which HMG‐I(Y) participates in repression of promoter activity. The effects of IL‐4 may include derepression at this site.

Original languageEnglish (US)
Pages (from-to)798-808
Number of pages11
JournalEuropean Journal of Immunology
Volume25
Issue number3
DOIs
StatePublished - Mar 1995
Externally publishedYes

Keywords

  • Gene transcription
  • Germ‐line Ig promoters
  • HMG‐I(Y)
  • IgE switch regulation
  • Interleukin‐4

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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