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STAT5‐induced Id‐1 transcription involves recruitment of HDAC1 and deacetylation of C/EBPβ
Author(s) -
Xu Min,
Nie Lei,
Kim SeungHwan,
Sun XiaoHong
Publication year - 2003
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1093/emboj/cdg094
Subject(s) - library science , foundation (evidence) , history , archaeology , computer science
Transcriptional activation is associated commonly with recruitment of histone acetylases, while repression involves histone deacetylases (HDACs). Here, we provide evidence to suggest that STAT5 activates gene expression by recruiting HDAC. The interleukin‐3 (IL‐3)‐dependent expression of the Id‐1 gene, encoding a helix–loop–helix (HLH) transcriptional inhibitor, is activated by both C/EBPβ and STAT5 transcription factors bound to its pro‐B‐cell enhancer (PBE), but is inhibited by HDAC inhibitors in Ba/F3 cells. STAT5 interacts with HDAC1 in the PBE region, resulting in deacetylation of histones, as well as C/EBPβ, whose acetylation diminishes its DNA‐binding activity. Consistently, expression of an acetylation‐resistant mutant of C/EBPβ results in IL‐3‐independent expression of the Id‐1 gene. Thus, we propose a novel mechanism by which STAT5 mediates the deacetylation of C/EBPβ, allowing transcriptional activation.