Defective GATA-3 expression in Th2 LCR-deficient mice

Soo Seok Hwang; Kiwan Kim; Gap Ryol Lee

doi:10.1016/j.bbrc.2011.06.080

Defective GATA-3 expression in Th2 LCR-deficient mice

Biochem Biophys Res Commun. 2011 Jul 15;410(4):866-71. doi: 10.1016/j.bbrc.2011.06.080. Epub 2011 Jun 15.

Authors

Soo Seok Hwang¹, Kiwan Kim, Gap Ryol Lee

Affiliation

¹ Department of Life Science, Sogang University, Seoul 121-742, Republic of Korea.

PMID: 21703230
DOI: 10.1016/j.bbrc.2011.06.080

Abstract

Th2 cell differentiation is critically influenced by transcription factor GATA-3 and by various cis-acting elements including enhancers, silencers and a locus control region (LCR) in the Th2 cytokine locus. Th2 LCR-deficient Th2 cells completely lost the expression of GATA-3 and the phosphorylation of STAT6. Histone 3 lysine 4 (H3-K4) was hypomethylated in the gata3 locus in these cells. GATA-3 and STAT6 bound several regulatory regions in the gata3 locus and transactivated the expression of the gata3 gene. These results suggest that Th2 differentiation program stimulates feed-forward regulation of gata3 gene expression.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Animals
Cell Differentiation / genetics*
GATA3 Transcription Factor / genetics*
Locus Control Region / genetics*
Mice
Mice, Mutant Strains
Phosphorylation
STAT6 Transcription Factor / metabolism
Th2 Cells / cytology*
Th2 Cells / metabolism
Transcriptional Activation*

Substances

GATA3 Transcription Factor
Gata3 protein, mouse
STAT6 Transcription Factor
Stat6 protein, mouse