Gfi1-mediated stabilization of GATA3 protein is required for Th2 cell differentiation

J Biol Chem. 2008 Oct 17;283(42):28216-25. doi: 10.1074/jbc.M804174200. Epub 2008 Aug 13.

Abstract

The differentiation of naive CD4 T cells into Th2 cells requires the T cell receptor-mediated activation of the ERK MAPK cascade. Little is known, however, in regard to how the ERK MAPK cascade regulates Th2 cell differentiation. We herein identified Gfi1 (growth factor independent-1) as a downstream target of the ERK MAPK cascade for Th2 cell differentiation. In the absence of Gfi1, interleukin-5 production and the change of histone modification at the interleukin-5 gene locus were severely impaired. Furthermore, the interferon gamma gene showed a striking activation in the Gfi1(-/-) Th2 cells. An enhanced ubiquitin/proteasome-dependent degradation of GATA3 protein was observed in Gfi1(-/-) Th2 cells, and the overexpression of GATA3 eliminated the defect of Th2 cell function in Gfi1-deficient Th2 cells. These data suggest that the T cell receptor-mediated induction of Gfi1 controls Th2 cell differentiation through the regulation of GATA3 protein stability.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Differentiation
  • DNA-Binding Proteins / metabolism*
  • GATA3 Transcription Factor / metabolism*
  • Gene Expression Regulation*
  • Humans
  • Interleukin-5 / metabolism
  • MAP Kinase Signaling System
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Models, Biological
  • Proteasome Endopeptidase Complex / metabolism
  • Th2 Cells / metabolism*
  • Transcription Factors / metabolism*
  • Ubiquitin / chemistry

Substances

  • DNA-Binding Proteins
  • GATA3 Transcription Factor
  • Gata3 protein, mouse
  • Gfi1 protein, mouse
  • Interleukin-5
  • Transcription Factors
  • Ubiquitin
  • Proteasome Endopeptidase Complex